bims-caglex Biomed News
on Cellular aging and life extension
Issue of 2024–10–20
sixty-five papers selected by
Mario Alexander Guerra Patiño, Universidad Antonio Nariño



  1. Int J Biol Macromol. 2024 Oct 15. pii: S0141-8130(24)07418-X. [Epub ahead of print] 136610
      Aging is an irreversible and continuous biological process involving intricate and interconnected mechanisms. The present work is focused on unravelling the anti-aging mechanisms of mealworm protein and protein-enriched fruit bar and vegetable soup in D-galactose-induced aged mice. Mealworm protein and enriched products significantly enhanced body weight, organ indices, and gut health. Behavioral assessments reflected enhanced neuroprotective effects. Mealworm protein and its enriched products demonstrated protective effects through anti-inflammatory activity with the highest reduction of TNFα (17.1 %), IL-6 (55.5 %), and IL-1β (75.1 %) levels and upregulated the anti-inflammatory marker (IL-4). Gene expression studies confirmed the induction of anti-aging effects by promoting metabolism, reducing cellular senescence, and enhancing anti-oxidant enzyme activity. The treatments extended telomere lengths by 3-4 times, further affirming the potential anti-aging efficacy of mealworm protein and its enriched products. Mealworm protein demonstrated positive effects on weight gain, anti-inflammatory responses, and telomere length; while fruit and vegetable products enhanced antioxidant activity, and positively influenced gut health. Further, a synergistic effect was observed by combining them, which resulted in improved overall anti-aging effect. The present work provides valuable insights into the multifaceted anti-aging mechanisms associated with mealworm protein and enriched products, highlighting their potential as functional foods with significant health-promoting effects.
    Keywords:  D-galactose-induced aged mice; Gut microbiota; Inflammation; Mealworm protein; Protein-enriched fruit bar; Protein-enriched vegetable soup
    DOI:  https://doi.org/10.1016/j.ijbiomac.2024.136610
  2. Phytomedicine. 2024 Oct 05. pii: S0944-7113(24)00788-8. [Epub ahead of print]135 156131
       BACKGROUND: Accumulation of senescent cells in tissues and their downstream effect programs have emerged as key drivers of aging and age-associated pathologies. Recent progresses in senotherapeutics indicated that either selectively killing senescent cells with senolytics or suppressing the senescence-associated secretory phenotype (SASP) secretion using senomorphics contributes to extending of the healthy lifespan and alleviating numerous age-related disorders in mice.
    PURPOSE: However, the potential side-effects and long-term cytotoxicity of the above novel compounds have not yet been determined. Therefore, it seems to be more efficient to explore new senotherapeutical functions from approved drugs.
    METHODS: The effects of valproic acid (VPA), a derivative of valine, in cellular senescence were evaluated by senescence-associated β galactosidase (SA-β-Gal) staining, flow cytometry and western blot (WB). The cell viability was tested using CCK-8 kits. Cell apoptosis was detected by Annexin V-EGFP/PI apoptosis detection kit. Cell autophagy was checked using GFP-RFP-LC3 ratiometric plasmid. The roles of VPA in lung aging were investigated by in vivo experiments using H&E and Masson staining, WB, as well as electronic microscope strategies.
    RESULTS: Here we identified VPA was able to induce an over-accumulation of reactive oxygen species (ROS) (>1.5 times increasing) and apoptosis (>2 times increasing) of senescent cells. Mechanistically, VPA activated the phospholipid modifying enzyme membrane-bound O-acyltransferase domain-containing protein 1 (MBOAT1), which was repressed during senescence, then promoted mitochondrial autophagy and apoptosis. In addition, VPA was also found to alleviate therapy induced abnormal mitochondria and lung aging phenotype (>1.5 times decreasing of lung fibrosis markers and >2.5 times increasing of naïve/memory CD4+ or CD8+ T cells) in vivo.
    CONCLUSION: Taken together, our study demonstrated that VPA was able to selectively kill senescent cells both in vitro and in vivo, and thus shedding light on new functions and novel potential application of VPA in anti-aging and anti-age-associated diseases.
    Keywords:  Cellular senescence; Mitochondria; ROS; SASP
    DOI:  https://doi.org/10.1016/j.phymed.2024.156131
  3. Nutrients. 2024 Sep 29. pii: 3305. [Epub ahead of print]16(19):
      Background: Aging is a natural biological process influenced by multiple factors and is a significant contributor to various chronic diseases. Slowing down the aging process and extending health span have been pursuits of the scientific field. Methods: Examination of the effects of dietary polyphenols on hallmarks of aging such as genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis. Results: Polyphenols, abundant in nature, exhibit numerous biological activities, including antioxidant effects, free radical scavenging, neuroprotection, and anti-aging properties. These compounds are generally safe and effective in potentially slowing aging and preventing age-related disorders. Conclusions: The review encourages the development of novel therapeutic strategies using dietary polyphenols to create holistic anti-aging therapies and nutritional supplements.
    Keywords:  anti-aging; polyphenol; the hallmarks of aging
    DOI:  https://doi.org/10.3390/nu16193305
  4. Cell Mol Neurobiol. 2024 Oct 16. 44(1): 67
      Aging, an inevitable physiological process leading to a progressive decline in bodily functions, has been an abundantly researched domain with studies attempting to slow it down and reduce its debilitating effects. Investigations into the cellular and molecular pathways associated with aging have allowed the formulation of therapeutic strategies. Of these, caloric restriction (CR) has been implicated for its role in promoting healthy aging by modulating key molecular targets like Insulin/IGF-1, mTOR, and sirtuins. However, CR requires dedication and commitment to a strict regimen which poses a difficulty in maintaining consistency. To maneuver around cumbersome diets, Caloric Restriction Mimetics (CRMs) have emerged as promising alternatives by mimicking the beneficial effects of CR. This review elucidates the molecular foundations enabling CRMs like rapamycin, metformin, resveratrol, spermidine, and many more to function as suitable anti-aging molecules. Moreover, it explores clinical trials (retrieved from the clinicaltrials.gov database) aimed at demonstrating the efficacy of CRMs as effective candidates against age-related neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
    Keywords:  Aging; Alzheimer’s disease; CR-mimetics; Caloric restriction; Clinical trials; Parkinson’s disease
    DOI:  https://doi.org/10.1007/s10571-024-01493-2
  5. Clin Cosmet Investig Dermatol. 2024 ;17 2243-2259
       Background: Skin aging is the most obvious feature of human aging, and delaying aging has become a hot and difficult research topic in aesthetic medicine. The accumulation of dysfunctional senescent cells is one of the important mechanisms of skin aging, based on which a series of anti-aging strategies have been generated. In this paper, from the perspective of cellular senescence, we utilize bibliometrics and research review to explore the research hotspots and trends in this field, with a view to providing references for skin health and aesthetic medicine.
    Methods: We obtained literature related to this field from the Web of Science Core Collection database from 1994 to 2024. Bibliometrix packages in R, CiteSpace, VOSviewer, Origin, and Scimago Graphica were utilized for data mining and visualization.
    Results: A total of 2,796 documents were included in the analysis. The overall trend of publications showed a continuous and rapid increase from 2016-2023, but the total citations improved poorly over time. In this field, Journal of Cosmetic Dermatology, Journal of Investigative Dermatology, Experimental Gerontology are core journals. Kim J, Lee JH, Lee S, Rattan SIS, Chung JH and Kim JH are the core authors in this field. Seoul National University is the first in terms of publications. Korea is the country with the most publications, but USA has the most total citations. Top 10 keywords include: gene-expression, skin, cellular senescence, cell, oxidative stress, antioxidants, in vitro, fibroblasts, mechanism, cancer. Current research trends are focused on neurodegeneration, skin rejuvenation, molecular docking, fibrosis, wound healing, SASP, skin barrier, and antioxidants. The core literature and references reflect topics such as the major molecular pathways in the aging process, and the relationship with tumors.
    Conclusion: This field of research has been rapidly rising in recent years. Relevant research hotspots focus on oxidative stress, fibroblasts, and senescence-associated secretory phenotype. Anti-aging strategies targeting cellular senescence hold great promise, including removal of senescent cells or attenuation of SASP factors, corresponding to senolytics and senomorphics therapies, respectively.
    Keywords:  aesthetic medicine; anti-aging; cellular senescence; senolytic; skin aging
    DOI:  https://doi.org/10.2147/CCID.S403417
  6. J Agric Food Chem. 2024 Oct 14.
      Human skin aging, a complex process influenced by intrinsic aging and extrinsic photoaging, is marked by the accumulation of reactive oxygen species (ROS) that cause DNA damage, impaired dermal fibroblast function, and wrinkle formation. External stressors, such as ultraviolet (UV) radiation, can trigger cellular senescence. Sirtuin-1 (SIRT1), an NAD+-dependent enzyme in the sirtuin family, plays a crucial role in deacetylating p53, thereby inhibiting its nuclear translocation and reducing skin senescence. Galangin, a flavonoid found in honey and Alpinia officinarum root, has antioxidant and anti-inflammatory properties. This study investigates the protective mechanism of galangin against UVB-induced senescence in human dermal fibroblasts (HDFs) by examining its effects on SIRT1 and its target, acetylated-p53. An in vitro model of UVB-induced senescence using HDFs and an in vivo model using nude mice were employed to assess the dermal protective effects of galangin. The results demonstrate that while UVB exposure does not decrease SIRT1 protein levels, it impairs its enzymatic function. However, galangin treatment counteracts these adverse effects. Additionally, UVB exposure significantly reduces cell viability and upregulates senescence markers like p16, p21, and p53 nuclear transactivation. An increase in senescence-associated β-galactosidase (SA-β-gal) positive cells was observed in UVB-exposed dermal fibroblasts. Galangin treatment mitigates UVB-induced cellular senescence by enhancing SIRT1-mediated p53 deacetylation, thereby inhibiting nuclear translocation and reducing dermal senescence. These findings suggest that galangin is a promising agent for alleviating UVB-induced skin aging and could be a potential component in antiaging cosmetic formulations.
    Keywords:  SIRT1; galangin; human dermal fibroblasts; p53; photoaging
    DOI:  https://doi.org/10.1021/acs.jafc.4c05945
  7. Chin Med J Pulm Crit Care Med. 2024 Sep;2(3): 133-141
      Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease characterized by airflow limitation and changes in airway structures that can lead to chronic bronchitis, small airway diseases, and emphysema. COPD is the 3rd leading cause of death worldwide and despite current research, there are no curative disease treatments for COPD. As the prevalence of COPD is higher in people over 60 years old than in younger age groups, COPD is considered a condition of accelerated lung aging. Natural lung aging is associated with molecular, cellular, and physiological changes that cause alteration in lung structure, in lung function and regeneration, and decreased immune system response that could lead to lung disease like COPD. Mechanisms of accelerated lung aging are complex and composed by increased oxidative stress induced by exposure to cigarette smoke, by chronic inflammatory processes, and increased number of senescent cells within the airways. Cellular senescence is the cessation of cell division after a finite number of proliferation cycles or in response to cell stressors, such as oxidative stress. Senescent cells show activation of the cell cycle regulators p21CIP1 (cyclin-dependent kinase inhibitor-1), p16INK4 (cyclin-dependent kinase inhibitor-2A), and p53 (cellular tumor antigen p53) that lead to cell cycle arrest. Senescent cells exhibit a change in their phenotype and their metabolic activity, along with the production of proinflammatory proteins collectively known as senescence-associated secretory phenotype (SASP). This review aims to describe recent developments in our understanding of aging mechanisms and how the acceleration of lung aging participates in COPD pathophysiology and comorbidities. Understanding and targeting aging mechanisms may result in the development of new therapeutics that could be effective for COPD and also for other age-related diseases.
    Keywords:  Aging; Cellular senescence; Chronic obstructive pulmonary disease; MicroRNAs; Senescence-associated secretory phenotype
    DOI:  https://doi.org/10.1016/j.pccm.2024.08.007
  8. Biochimie. 2024 Oct 15. pii: S0300-9084(24)00235-9. [Epub ahead of print]
      Aging is a degenerative, biological, and time-dependent process that affects all organisms. Yeast aging is a physiological phenomenon characterized by the progressive transformation of yeast cells, resulting in modifications to their viability and vitality. Aging in yeast cells is comparable to that in higher organisms in some respects; however, due to their straightforward and well-characterized genetic makeup, these cells present unique advantages when it comes to researching the aging process. Here, we assessed the impact of human anti-apoptotic Bcl-2 and Bcl-xL proteins on aging using a yeast model. The findings clearly showed that these proteins exhibited remarkable anti-aging properties in yeast cells. Our data indicate that the presence of both proteins enhanced the reproductive survival of aging cells, likely by effecting the components functioning as both pro- and anti-oxidants, depending on the stage of yeast cell lifespan. Both proteins partially protected yeast cells from aging-related morphological deformations and cellular damage during the aging period. In particular, Bcl-xL expressing yeast cells reached the maximum activity levels for almost all of the major antioxidant enzymes and the total antioxidant status on the 8th day of lifespan and could provide effective protection at the latest stage of the investigated aging period. The chemometric data analysis of IR spectra confirmed the findings of the morphological and biochemical analyses. In this regard, specifically, understanding the mechanism of action on the cellular redox state of Bcl-xL in yeast may facilitate comprehension of its indirect antioxidant function in higher eukaryotes.
    Keywords:  Aging; Anti-apoptotic proteins of Bcl-2 family; Antioxidant system; Biochemical make-up; Oxidative stress; Yeast
    DOI:  https://doi.org/10.1016/j.biochi.2024.10.009
  9. Aging Cell. 2024 Sep;23(9): e14240
      The number of senescent vascular endothelial cells increases during aging and their dysfunctional phenotype contributes to age-related cardiovascular disease. Identification of senescent cells is challenging as molecular changes are often tissue specific and occur amongst clusters of normal cells. Here, we established, benchmarked, and validated a new gene signature called EndoSEN that pinpoints senescent endothelial cells. The EndoSEN signature was enriched for interferon-stimulated genes (ISG) and correlated with the senescence-associated secretory phenotype (SASP). SASP establishment is classically attributed to DNA damage and cyclic GMP-AMP synthase activation, but our results revealed a pivotal role for RNA accumulation and sensing in senescent endothelial cells. Mechanistically, we showed that endothelial cell senescence hallmarks include self-RNA accumulation, RNA sensor RIG-I upregulation, and an ISG signature. Moreover, a virtual model of RIG-I knockout in endothelial cells underscored senescence as a key pathway regulated by this sensor. We tested and confirmed that RIG-I knockdown was sufficient to extend the lifespan and decrease the SASP in endothelial cells. Taken together, our evidence suggests that targeting RNA sensing is a potential strategy to delay vascular aging.
    Keywords:  RNA sensing; cardiovascular diseases; cellular senescence; endothelial cells; senescence‐associated secretory phenotype
    DOI:  https://doi.org/10.1111/acel.14240
  10. Aging Biol. 2023 ;pii: 20230005. [Epub ahead of print]1(1):
      Somatic mutations accumulate in multiple organs and tissues during aging and are a known cause of cancer. Cellular senescence is a possible cause of functional decline in aging, yet also acts as an anticancer mechanism in vivo. Here, we compared somatic mutation burden between early passage and deeply senescent human fibroblasts using single-cell whole-genome sequencing. The results show that single-nucleotide variants (SNVs) and small insertions and deletions (INDELs) are increased in senescent cells by about twofold but have the same mutational signature as early passage cells. The increase in SNVs and INDELs can be explained by increased replication errors due to the increased number of cell divisions senescent cells are likely to have undergone. By contrast, a stark increase of aneuploidies was observed in deeply senescent cells, with about half of all senescent cells affected but none of the early passage cells analyzed. These results indicate that large chromosomal events rather than small base substitutions or insertions and deletions could be mechanistically linked to cellular senescence.
    DOI:  https://doi.org/10.59368/agingbio.20230005
  11. Free Radic Biol Med. 2024 Oct 15. pii: S0891-5849(24)00970-5. [Epub ahead of print]
      With the development of the technology to generate transgenic and knockout mice in the 1990s, investigators had a powerful tool to directly test the impact of altering a specific gene on a biological process or disease. Over the past three decades, investigators have used transgenic and knockout mouse models, which have altered expression of antioxidant genes, to test the role of oxidative stress/damage in aging and age-related diseases. In this comprehensive review, we describe the studies using transgenic and knockout mouse models to test the role of oxidative stress/damage in aging (longevity) and three age-related diseases, e.g., sarcopenia, cardiac aging, and Alzheimer's Disease. While longevity was consistently altered only by one transgenic and one knockout mouse model as predicted by the Oxidative Stress Theory of Aging, the incidence/progression of the three age-related diseases (especially Alzheimer's disease) were robustly impacted when the expression of various antioxidant genes was altered using transgenic and knockout mouse models.
    Keywords:  Alzheimer’s Disease; Cardiac Aging; Lifespan; Oxidative Stress; Sarcopenia
    DOI:  https://doi.org/10.1016/j.freeradbiomed.2024.10.269
  12. Int J Mol Sci. 2024 Sep 30. pii: 10535. [Epub ahead of print]25(19):
      Progress made by the medical community in increasing lifespans comes with the costs of increasing the incidence and prevalence of age-related diseases, neurodegenerative ones included. Aging is associated with a series of morphological changes at the tissue and cellular levels in the brain, as well as impairments in signaling pathways and gene transcription, which lead to synaptic dysfunction and cognitive decline. Although we are not able to pinpoint the exact differences between healthy aging and neurodegeneration, research increasingly highlights the involvement of neuroinflammation and chronic systemic inflammation (inflammaging) in the development of age-associated impairments via a series of pathogenic cascades, triggered by dysfunctions of the circadian clock, gut dysbiosis, immunosenescence, or impaired cholinergic signaling. In addition, gender differences in the susceptibility and course of neurodegeneration that appear to be mediated by glial cells emphasize the need for future research in this area and an individualized therapeutic approach. Although rejuvenation research is still in its very early infancy, accumulated knowledge on the various signaling pathways involved in promoting cellular senescence opens the perspective of interfering with these pathways and preventing or delaying senescence.
    Keywords:  astrocytes; cellular senescence; immunosenescence; microglia; neuroinflammation; senescence-associated secretory phenotype
    DOI:  https://doi.org/10.3390/ijms251910535
  13. Ageing Res Rev. 2024 Oct 10. pii: S1568-1637(24)00348-9. [Epub ahead of print]101 102530
      Human aging is characterized by a gradual decline in physiological functions and an increased susceptibility to various diseases. The complex mechanisms underlying human aging are still not fully elucidated. Single-cell sequencing (SCS) technologies have revolutionized aging research by providing unprecedented resolution and detailed insights into cellular diversity and dynamics. In this review, we discuss the application of various SCS technologies in human aging research, encompassing single-cell, genomics, transcriptomics, epigenomics, and proteomics. We also discuss the combination of multiple omics layers within single cells and the integration of SCS technologies with advanced methodologies like spatial transcriptomics and mass spectrometry. These approaches have been essential in identifying aging biomarkers, elucidating signaling pathways associated with aging, discovering novel aging cell subpopulations, uncovering tissue-specific aging characteristics, and investigating aging-related diseases. Furthermore, we provide an overview of aging-related databases that offer valuable resources for enhancing our understanding of the human aging process.
    Keywords:  Aging-related diseases; Biomarkers; Human aging; Single-cell multi-omics; Single-cell sequencing
    DOI:  https://doi.org/10.1016/j.arr.2024.102530
  14. Mech Ageing Dev. 2024 Oct 11. pii: S0047-6374(24)00096-4. [Epub ahead of print]222 111996
      The aging process is a complex phenomenon characterised by a gradual decline in physiological functions and an increased susceptibility to age-related diseases. An important factor in aging is mitochondrial dysfunction, which leads to an accumulation of cellular damage over time. Mitochondrial Sirtuin 3 (Sirt3), an important regulator of energy metabolism, plays a central role in maintaining mitochondrial function. Loss of Sirt3 can lead to reduced energy levels and an impaired ability to repair cellular damage, a hallmark of the aging process. In this study we investigated the impact of Sirt3 loss on mitochondrial function, metabolic responses and cellular aging processes in male and female mouse embryonic fibroblasts (MEF) exposed to etoposide-induced DNA damage, which is commonly associated with cellular dysfunction and senescence. We found that Sirt3 contributes to the sex-specific metabolic response to etoposide treatment. While male MEF exhibited minimal damage suggesting potential prior adaptation to stress due to Sirt3 loss, female MEF lacking Sirt3 experienced higher vulnerability to genotoxic stress, implying a pivotal role of Sirt3 in their resistance to such challenges. These findings offer potential insights into therapeutic strategies targeting Sirt3- and sex-specific signalling pathways in diseases associated with DNA damage that play a critical role in the aging process.
    Keywords:  Aging; DNA damage; Etoposide; MEF; Sex differences; Sirtuin 3
    DOI:  https://doi.org/10.1016/j.mad.2024.111996
  15. Autophagy. 2024 Oct 14. 1-3
      Mitophagy, the selective autophagic clearance of damaged mitochondria, is considered vital for maintaining mitochondrial quality and cellular homeostasis; however, its molecular mechanisms, particularly under basal conditions, and its role in cellular physiology remain poorly characterized. We recently demonstrated that basal mitophagy is a key feature of primary human cells and is downregulated by immortalization, suggesting its dependence on the primary cell state. Mechanistically, we demonstrated that the PINK1-PRKN-SQSTM1 pathway regulates basal mitophagy, with SQSTM1 sensing superoxide-enriched mitochondria through its redox-sensitive cysteine residues, which mediate SQSTM1 oligomerization and mitophagy activation. We developed STOCK1N-57534, a small molecule that targets and promotes this SQSTM1 activation mechanism. Treatment with STOCK1N-57534 reactivates mitophagy downregulated in senescent and naturally aged donor-derived primary cells, improving cellular senescence(-like) phenotypes. Our findings highlight that basal mitophagy is protective against cellular senescence and aging, positioning its pharmacological reactivation as a promising anti-aging strategy.Abbreviation: IR: ionizing radiation; ROS: reactive oxygen species; SARs: selective autophagy receptors.
    Keywords:  Aging; SQSTM1/p62; autophagy; mitochondria; mitophagy; senescence
    DOI:  https://doi.org/10.1080/15548627.2024.2414461
  16. Aging Cell. 2024 Oct 15. e14348
      Aging is usually accompanied by excessive body fat gain, leading to increased susceptibility to comorbidities. This study aimed to explore an unexpected function for the eukaryotic initiation factor-2α (eIF2α) during aging. Reducing the eIF2α dose led to a reconfiguration of the metabolic equilibrium, promoting catabolism, facilitating lipolysis, and decreasing body fat accumulation while maintaining healthy glucose and lipid metabolism during aging. Specifically, eIF2α enhanced the expression of distinct messenger RNAs encoding mitochondrial electron transport chain proteins at the translation level. The mitochondrial respiration increased in eIF2α heterozygotes, even during aging. Deceleration of translation was demonstrated as a conserved mechanism for promoting longevity across various species. Our findings demonstrated that the restriction of translation by reducing eIF2α expression could fend off multiple tissue damage and improve metabolic homeostasis during aging. Hence, eIF2α was a crucial target for benefiting mammalian aging achieving delayed mammalian aging.
    Keywords:  ISR; aging; eIF2α; lipid metabolism; mitochondria; translation
    DOI:  https://doi.org/10.1111/acel.14348
  17. Aging (Albany NY). 2024 Oct 16. 16
    Yu-Xuan Lyu, Qiang Fu, Dominika Wilczok, Kejun Ying, Aaron King, Adam Antebi, Aleksandar Vojta, Alexandra Stolzing, Alexey Moskalev, Anastasia Georgievskaya, Andrea B Maier, Andrea Olsen, Anja Groth, Anna Katharina Simon, Anne Brunet, Aisyah Jamil, Anton Kulaga, Asif Bhatti, Benjamin Yaden, Bente Klarlund Pedersen, Björn Schumacher, Boris Djordjevic, Brian Kennedy, Chieh Chen, Christine Yuan Huang, Christoph U Correll, Coleen T Murphy, Collin Y Ewald, Danica Chen, Dario Riccardo Valenzano, Dariusz Sołdacki, David Erritzoe, David Meyer, David A Sinclair, Eduardo Nunes Chini, Emma C Teeling, Eric Morgen, Eric Verdin, Erik Vernet, Estefano Pinilla, Evandro F Fang, Evelyne Bischof, Evi M Mercken, Fabian Finger, Folkert Kuipers, Frank W Pun, Gabor Gyülveszi, Gabriele Civiletto, Garri Zmudze, Gil Blander, Harold A Pincus, Joshua McClure, James L Kirkland, James Peyer, Jamie N Justice, Jan Vijg, Jennifer R Gruhn, Jerry McLaughlin, Joan Mannick, João Passos, Joseph A Baur, Joe Betts-LaCroix, John M Sedivy, John R Speakman, Jordan Shlain, Julia von Maltzahn, Katrin I Andreasson, Kelsey Moody, Konstantinos Palikaras, Kristen Fortney, Laura J Niedernhofer, Lene Juel Rasmussen, Liesbeth M Veenhoff, Lisa Melton, Luigi Ferrucci, Marco Quarta, Maria Koval, Maria Marinova, Mark Hamalainen, Maximilian Unfried, Michael S Ringel, Milos Filipovic, Mourad Topors, Natalia Mitin, Nawal Roy, Nika Pintar, Nir Barzilai, Paolo Binetti, Parminder Singh, Paul Kohlhaas, Paul D Robbins, Paul Rubin, Peter O Fedichev, Petrina Kamya, Pura Muñoz-Canoves, Rafael de Cabo, Richard G A Faragher, Rob Konrad, Roberto Ripa, Robin Mansukhani, Sabrina Büttner, Sara A Wickström, Sebastian Brunemeier, Sergey Jakimov, Shan Luo, Sharon Rosenzweig-Lipson, Shih-Yin Tsai, Stefanie Dimmeler, Thomas A Rando, Tim R Peterson, Tina Woods, Tony Wyss-Coray, Toren Finkel, Tzipora Strauss, Vadim N Gladyshev, Valter D Longo, Varun B Dwaraka, Vera Gorbunova, Victoria A Acosta-Rodríguez, Vincenzo Sorrentino, Vittorio Sebastiano, Wenbin Li, Yousin Suh, Alex Zhavoronkov, Morten Scheibye-Knudsen, Daniela Bakula.
      The recent unprecedented progress in ageing research and drug discovery brings together fundamental research and clinical applications to advance the goal of promoting healthy longevity in the human population. We, from the gathering at the Aging Research and Drug Discovery Meeting in 2023, summarised the latest developments in healthspan biotechnology, with a particular emphasis on artificial intelligence (AI), biomarkers and clocks, geroscience, and clinical trials and interventions for healthy longevity. Moreover, we provide an overview of academic research and the biotech industry focused on targeting ageing as the root of age-related diseases to combat multimorbidity and extend healthspan. We propose that the integration of generative AI, cutting-edge biological technology, and longevity medicine is essential for extending the productive and healthy human lifespan.
    Keywords:  artificial intelligence; biotechnology; healthy longevity
    DOI:  https://doi.org/10.18632/aging.206135
  18. Mol Cell. 2024 Oct 17. pii: S1097-2765(24)00703-2. [Epub ahead of print]84(20): 3979-3996.e9
      Stimulator of interferon genes (STING) is activated in many pathophysiological conditions, leading to TBK1-dependent interferon production in higher organisms. However, primordial functions of STING independent of TBK1 are poorly understood. Here, through proteomics and bioinformatics approaches, we identify lysosomal biogenesis as an unexpected function of STING. Transcription factor EB (TFEB), an evolutionarily conserved regulator of lysosomal biogenesis and host defense, is activated by STING from multiple species, including humans, mice, and frogs. STING-mediated TFEB activation is independent of TBK1, but it requires STING trafficking and its conserved proton channel. GABARAP lipidation, stimulated by the channel of STING, is key for STING-dependent TFEB activation. STING stimulates global upregulation of TFEB-target genes, mediating lysosomal biogenesis and autophagy. TFEB supports cell survival during chronic sterile STING activation, a common condition in aging and age-related diseases. These results reveal a primordial function of STING in the biogenesis of lysosomes, essential organelles in immunity and cellular stress resistance.
    Keywords:  STING; STING channel; TBK1; TFE3; TFEB; autophagy; cGAS; chronic STING signaling; lysosome
    DOI:  https://doi.org/10.1016/j.molcel.2024.08.026
  19. bioRxiv. 2024 Oct 13. pii: 2024.10.11.617862. [Epub ahead of print]
      Cellular senescence, characterized by a permanent state of cell cycle arrest and a secretory phenotype contributing to inflammation and tissue deterioration, has emerged as a target for age-related interventions. Accumulation of senescent cells is closely linked with intervertebral disc (IVD) degeneration, a prevalent age-dependent chronic disorder causing low back pain. Previous studies have highlighted that platelet-derived growth factor (PDGF) mitigated IVD degeneration through anti-apoptosis, anti-inflammation, and pro-anabolism. However, its impact on IVD cell senescence remains elusive. In this study, human NP and AF cells derived from aged, degenerated IVDs were treated with recombinant human (rh) PDGF-AB/BB for 5 days and changes of transcriptome profiling were examined through mRNA sequencing. NP and AF cells demonstrated similar but distinct responses to the treatment. However, the effects of PDGF-AB and BB on human IVD cells were comparable. Specifically, PDGF-AB/BB treatment resulted in downregulation of gene clusters related to neurogenesis and response to mechanical stimulus in AF cells while the downregulated genes in NP cells were mainly associated with metabolic pathways. In both NP and AF cells, PDGF-AB and BB treatment upregulated the expression of genes involved in cell cycle regulation, mesenchymal cell differentiation, and response to reduced oxygen levels, while downregulating the expression of genes related to senescence associated phenotype, including oxidative stress, reactive oxygen species (ROS), and mitochondria dysfunction. Network analysis revealed that PDGFRA and IL6 were the top hub genes in treated NP cells. Furthermore, in irradiation-induced senescent NP cells, PDGFRA gene expression was significantly reduced compared to non-irradiated cells. However, rhPDGF-AB/BB treatment increased PDGFRA expression and mitigated the senescence progression through increased cell population in the S phase, reduced SA-β-Gal activity, and decreased expression of senescence related regulators including P21, P16, IL6, and NF-κB. Our findings reveal a novel anti-senescence role of PDGF in the IVD, demonstrating its ability to alleviate the senescent phenotype and protect against the progression of senescence. This makes it a promising candidate for preventing or treating IVD degeneration by targeting cellular senescence.
    Abstract Figure:
    DOI:  https://doi.org/10.1101/2024.10.11.617862
  20. Animals (Basel). 2024 Oct 08. pii: 2900. [Epub ahead of print]14(19):
      Brain aging in mammals is characterized by morphological and functional changes in neural cells. Macroscopically, this process, leading to progressive cerebral volume loss and functional decline, includes memory and motor neuron deficits, as well as behavioral disorders. Morphologically, brain aging is associated with aged neurons and astrocytes, appearing enlarged and flattened, and expressing enhanced pH-dependent β-galactosidase activity. Multiple mechanisms are considered hallmarks of cellular senescence in vitro, including cell cycle arrest, increased lysosomal activity, telomere shortening, oxidative stress, and DNA damage. The most common markers for senescence identification were identified in (i) proteins implicated in cell cycle arrest, such as p16, p21, and p53, (ii) increased lysosomal mass, and (iii) increased reactive oxygen species (ROS) and senescence-associated secretory phenotype (SASP) expression. Finally, dysfunctional autophagy, a process occurring during aging, contributes to altering brain homeostasis. The brains of mammals can be studied at cellular and subcellular levels to elucidate the mechanisms on the basis of age-related and degenerative disorders. The aim of this review is to summarize and update the most recent knowledge about brain aging through a comparative approach, where similarities and differences in some mammalian species are considered.
    Keywords:  brain aging; caloric restriction; mammals; metabolism; neural cells; nutrients
    DOI:  https://doi.org/10.3390/ani14192900
  21. Trends Genet. 2024 Oct 17. pii: S0168-9525(24)00214-2. [Epub ahead of print]
      Research into aging constitutes a pivotal endeavor aimed at elucidating the underlying biological mechanisms governing aging and age-associated diseases, as well as promoting healthy longevity. Recent advances in transcriptomic technologies, such as bulk RNA sequencing (RNA-seq), single-cell transcriptomics, and spatial transcriptomics, have revolutionized our ability to study aging at unprecedented resolution and scale. These technologies present novel opportunities for the discovery of biomarkers, elucidation of molecular pathways, and development of targeted therapeutic strategies for age-related disorders. This review surveys recent breakthroughs in different types of transcripts on aging, such as mRNA, long noncoding (lnc)RNA, tRNA, and miRNA, highlighting key findings and discussing their potential implications for future studies in this field.
    Keywords:  aging; bulk RNA-seq; single-cell transcriptomics; spatial transcriptomics; transcriptomics
    DOI:  https://doi.org/10.1016/j.tig.2024.09.006
  22. Int J Mol Sci. 2024 Oct 01. pii: 10593. [Epub ahead of print]25(19):
      Retrotransposons are mobile DNA elements that are more active with increasing age and exacerbate aging phenotypes in multiple species. We previously reported an unexpected extension of chronological lifespan in the yeast, Saccharomyces paradoxus, due to the presence of Ty1 retrotransposons when cells were aged under conditions of mild stress. In this study, we tested a subset of genes identified by RNA-seq to be differentially expressed in S. paradoxus strains with a high-copy number of Ty1 retrotransposons compared with a strain with no retrotransposons and additional candidate genes for their contribution to lifespan extension when cells were exposed to a moderate dose of hydroxyurea (HU). Deletion of ADE8, NCS2, or TRM9 prevented lifespan extension, while deletion of CDD1, HAC1, or IRE1 partially prevented lifespan extension. Genes overexpressed in high-copy Ty1 strains did not typically have Ty1 insertions in their promoter regions. We found that silencing genomic copies of Ty1 prevented lifespan extension, while expression of Ty1 from a high-copy plasmid extended lifespan in medium with HU or synthetic medium. These results indicate that cells adapt to expression of retrotransposons by changing gene expression in a manner that can better prepare them to remain healthy under mild stress.
    Keywords:  Saccharomyces; Ty1; aging; chronological lifespan; retrotransposon; yeast
    DOI:  https://doi.org/10.3390/ijms251910593
  23. Sci Rep. 2024 10 13. 14(1): 23920
      Our research explores the detrimental effects of microplastic (MP) exposure on adipose tissue aging and function, emphasizing the potential health risks associated with environmental pollutants. Utilizing both in vivo and in vitro models, we discovered that MPs accumulate in adipose tissues, leading to cellular senescence, inflammation, and hindered adipogenic differentiation. Notably, our findings demonstrate that MPs prompt an aging response in both epididymal and inguinal white adipose tissue, increase senescence-associated β-galactosidase activity, and upregulate key senescence and inflammatory markers. Furthermore, we show that MPs disrupt normal adipogenic differentiation by reducing lipid droplet formation and downregulating critical adipogenic markers. These insights highlight the urgent need for further investigation into the long-term consequences of MP pollution on biological aging and underscore the importance of developing public health strategies to mitigate these effects.
    Keywords:  Adipose tissue; Differentiation; Inflammation; Microplastic; Senescence
    DOI:  https://doi.org/10.1038/s41598-024-74892-6
  24. Nat Commun. 2024 Oct 17. 15(1): 8960
      Appropriate repair of damaged DNA and the suppression of DNA damage responses at telomeres are essential to preserve genome stability. DNA damage response (DDR) signaling consists of cascades of kinase-driven phosphorylation events, fine-tuned by proteolytic and regulatory ubiquitination. It is not fully understood how crosstalk between these two major classes of post-translational modifications impact DNA repair at deprotected telomeres. Hence, we performed a functional genetic screen to search for ubiquitin system factors that promote KAP1S824 phosphorylation, a robust DDR marker at deprotected telomeres. We identified that the OTU family deubiquitinase (DUB) OTUD5 promotes KAP1S824 phosphorylation by facilitating ATM activation, through stabilization of the ubiquitin ligase UBR5 that is required for DNA damage-induced ATM activity. Loss of OTUD5 impairs KAP1S824 phosphorylation, which suppresses end-joining mediated DNA repair at deprotected telomeres and at DNA breaks in heterochromatin. Moreover, we identified an unexpected role for the heterochromatin factor KAP1 in suppressing DNA repair at telomeres. Altogether our work reveals an important role for OTUD5 and KAP1 in relaying DDR-dependent kinase signaling to the control of DNA repair at telomeres and heterochromatin.
    DOI:  https://doi.org/10.1038/s41467-024-53404-0
  25. J Ethnopharmacol. 2024 Oct 14. pii: S0378-8741(24)01242-X. [Epub ahead of print] 118943
       ETHNOPHARMACOLOGICAL RELEVANCE: As one of the important by-products of Taxus chinensis (Pilg.) Rehder, its fruit (TCF) has a sweet taste, which is commonly used in folklore to make health care wine reputed for enhancing immune function and promoting anti-aging effects, especially popular in the longevity villages of China for a long history. Evidences had showed that Taxus chinensis fruit contained polysaccharides, flavonoids, amino acids and terpenoids, which all were free of toxic compounds , but its medicinal value has not been fully recognized. Our previous studies have found that TCF extract may reverse many biological events, including oxidative stress, inflammatory response, neuronal apoptosis, etc. by in silico methods, suggesting potential avenues for future pharmaceutical exploration in aging and age-related diseases.
    AIM OF THE STUDY: Yet, the anti-aging properties of TCF have not been specifically studied, this study aims to fill this gap by investigating the effects of TCF extract (TCFE) in an aging mouse model, particularly focusing on its role in inhibiting microglial activation and elucidating its underlying anti-aging mechanisms.
    MATERIALS AND METHODS: An aging mouse model was induced using D-galactose, with interventions involving high, medium, and low doses of TCFE compared to a positive control (2mg/kg rapamycin combined with 100mg/kg metformin). The methodology involved evaluating behavioral changes, serum oxidative and antioxidative markers, hypothalamic β-galactosidase activity, expression of the aging-related protein P63, serum inflammatory factors, and the TLR4/NF-κB/NLRP3 inflammatory pathway in hypothalamic tissues. Additionally, to strengthen our in vivo findings, we conducted in vitro experiments on LPS-stimulated BV2 microglial cells. Finally, UPLC-MS/MS for precise component analysis using compound standards, coupled with molecular docking analyses, were employed to discern and elucidate the anti-inflammatory mechanisms of TCF.
    RESULTS: In vivo results revealed TCFE significantly ameliorated behavioral deficits, reduced oxidative stress markers (MDA) and pro-inflammatory cytokines (IL1-β, IL-6, IFNg, TNFα, IL-17), and increased in antioxidants (SOD, T-AOC) and anti-inflammatory factors (IL-10). TCFE also reduced hypothalamic senescence, improved cellular integrity, lowered p63, and inhibited microglia activation and inflammatory pathways (TLR4, NFKB, NLRP3). The overall effect of TCFE was better than that of the positive drug group (rapamycin combined with metformin). In vitro results further revealed that TCFE markedly decreased IL1-β, NFKB, and TLR4 levels in BV2 microglial cells, showing comparable efficacy to a TLR4 classic positive inhibitor C34, supporting its anti-inflammatory role. Through UPLC-MS/MS analysis coupled with compound standards, we identified ten bioactive compounds, including gallocatechin, epigallocatechin, catechin, procyanidin B2, kaempferol, quercetin, rutin, naringin, apigenin, ginkgetin. All these compounds showed strong binding affinity to TLR4, notably procyanidin B2 and rutin, potentially through hydrogen bonds, aromatic cation-π interactions, and hydrophobic interactions, suggesting a molecular basis for their anti-inflammatory action.
    CONCLUSION: TCFE showed strong anti-aging effects by inhibiting microglia activation and lessening oxidative stress and modulating inflammatory pathways. This research supports TCF's use in anti-aging and sets a base for future drug development in the realms of neuroinflammation and aging.
    Keywords:  TLR4; Taxus chinensis fruit; aging; anti-inflammation; microglia activation
    DOI:  https://doi.org/10.1016/j.jep.2024.118943
  26. J Cereb Blood Flow Metab. 2024 Oct 18. 271678X241289780
      Aging-related cognitive decline is emerging as a health concern during the aging process of the global population. Hahn and colleagues found that glial aging was particularly accelerated in white matter compared to cortical regions. Specialized neuronal populations showed region-specific changes in gene expression. Acute dietary restriction triggers a reprogramming of genes associated with the circadian clock in glial cells, whereas injections of young mouse plasma selectively reverse age-related expression patterns. The discovery of region-specific aging could enhance our understanding of the aging process and offer new possibilities for innovative treatment strategies and interventions for cognitive impairments related to aging.
    Keywords:  Aging; brain region; cognitive decline; microglia; white matter
    DOI:  https://doi.org/10.1177/0271678X241289780
  27. Cells. 2024 Sep 26. pii: 1611. [Epub ahead of print]13(19):
      The constant increase in the elderly population presents significant challenges in addressing new social, economic, and health problems concerning this population. With respect to health, aging is a primary risk factor for age-related diseases, which are driven by interconnected molecular hallmarks that influence the development of these diseases. One of the main mechanisms that has attracted more attention to aging is autophagy, a catabolic process that removes and recycles damaged or dysfunctional cell components to preserve cell viability. The autophagy process can be induced or deregulated in response to a wide range of internal or external stimuli, such as starvation, oxidative stress, hypoxia, damaged organelles, infectious pathogens, and aging. Natural compounds that promote the stimulation of autophagy regulatory pathways, such as mTOR, FoxO1/3, AMPK, and Sirt1, lead to increased levels of essential proteins such as Beclin-1 and LC3, as well as a decrease in p62. These changes indicate the activation of autophagic flux, which is known to be decreased in cardiovascular diseases, neurodegeneration, and cataracts. The regulated administration of natural compounds offers an adjuvant therapeutic alternative in age-related diseases; however, more experimental evidence is needed to support and confirm these health benefits. Hence, this review aims to highlight the potential benefits of natural compounds in regulating autophagy pathways as an alternative approach to combating age-related diseases.
    Keywords:  age-related diseases; autophagy; cardiopathies; cataract; natural compounds; neurodegeneration
    DOI:  https://doi.org/10.3390/cells13191611
  28. J Med Chem. 2024 Oct 17.
      Inhibition of the protein-protein interaction between Kelch-like ECH-associated protein 1 (Keap1) and nuclear factor erythroid 2-related factor 2 (Nrf2) has been recognized as an attractive approach for treating oxidative stress-related diseases. Here, we present a new series of noncovalent Keap1-Nrf2 inhibitors developed by a conformational restriction strategy of our fluorenone-based compounds previously identified by fragment-based drug discovery. The design was guided by X-ray cocrystal structures, and the subsequent optimization process aimed at improving affinity, cellular activity, and metabolic stability. From the noncyclic compound 7 (Ki = 2.9 μM), a new series of tetrahydroisoquinoline-based Keap1 inhibitors with up to 223-fold improvement in binding affinity (57, Ki = 13 nM), better metabolic stability, and enhanced cellular activity was obtained. In addition, the compounds showed selectivity for the Keap1 Kelch domain across a panel of 15 homologous proteins. We thereby demonstrate the utility of cyclic rigidification in the design of potent and more drug-like Keap1-Nrf2 inhibitors.
    DOI:  https://doi.org/10.1021/acs.jmedchem.4c01221
  29. J Agric Food Chem. 2024 Oct 17.
      T-2 toxin induces cell immunotoxicity by triggering an intracellular hypoxic microenvironment and activates hypoxia-inducible factor-1α (HIF-1α), which exerts cellular protective effects. Mycotoxins can also induce senescence. The aging of immune function, termed "immunosenescence," is an important factor in the decline of biological immunity and accelerates senescence. However, the mechanism underlying T-2 toxin-induced immunosenescence remains unclear. This study aimed to elucidate the roles of HIF-1α and cGAS-STING signaling in this process and uncover the mechanisms through which T-2 toxin impacts cytoskeletal integrity and cellular senescence using a RAW264.7 macrophage model. The cells were treated with T-2 toxin (14 nM) for 1-24 h. We revealed that T-2 toxin-induced immunosenescence in RAW264.7 cells by activating the HIF-1α/cGAS-STING axis. The cGAS-STING pathway promotes cell senescence and apoptosis; however, we revealed that HIF-1α negatively regulated this pathway, thereby inhibiting cellular senescence and apoptosis. However, PARP 1 cleavage by caspase 3/9 inhibited DNA repair and accelerated the transition from senescence to apoptosis. At the late stages of T-2 toxin exposure (12 h), HIF-1α accelerated cellular senescence by disrupting the dynamic balance of cytoskeletal α-tubulin and F-actin and destabilizing the cytoskeletal structure. Our research demonstrates that T-2 toxin induces immunosenescence in RAW264.7 cells by activating the cGAS-STING pathway, with HIF-1α signaling serving as a negative regulator. This study provides a deeper understanding of T-2 toxin-induced immunosenescence.
    Keywords:  HIF-1α; PARP 1; T-2 toxin; cGAS-STING; immunosenescence
    DOI:  https://doi.org/10.1021/acs.jafc.4c07268
  30. J Asian Nat Prod Res. 2024 Oct 15. 1-14
      The global aging population highlights the need for effective anti-aging treatments. Natural products show promise, but thorough evaluation requires in vivo models due to the complexity of aging. Ethical concerns are driving a shift from traditional models like rabbits and mice to alternatives such as Caenorhabditis elegans. This microscopic nematode, with its short life cycle, genetic similarities to humans, and cost-effectiveness, is ideal for testing anti-aging compounds. We review studies using C. elegans to assess natural products, suggesting it could serve as a primary model for -evaluating the safety and efficacy of plant-derived anti-aging compounds.
    Keywords:  Aging; C. elegans; in vivo model; natural products
    DOI:  https://doi.org/10.1080/10286020.2024.2414189
  31. Int J Mol Sci. 2024 Sep 27. pii: 10405. [Epub ahead of print]25(19):
      Targeting DNA repair pathways is an important strategy in anticancer therapy. However, the unrevealed interactions between different DNA repair systems may interfere with the desired therapeutic effect. Among DNA repair systems, BER and NHEJ protect genome integrity through the entire cell cycle. BER is involved in the repair of DNA base lesions and DNA single-strand breaks (SSBs), while NHEJ is responsible for the repair of DNA double-strand breaks (DSBs). Previously, we showed that BER deficiency leads to downregulation of NHEJ gene expression. Here, we studied BER's response to NHEJ deficiency induced by knockdown of NHEJ scaffold protein XRCC4 and compared the knockdown effects in normal (TIG-1) and hTERT-modified cells (NBE1). We investigated the expression of the XRCC1, LIG3, and APE1 genes of BER and LIG4; the Ku70/Ku80 genes of NHEJ at the mRNA and protein levels; as well as p53, Sp1 and PARP1. We found that, in both cell lines, XRCC4 knockdown leads to a decrease in the mRNA levels of both BER and NHEJ genes, though the effect on protein level is not uniform. XRCC4 knockdown caused an increase in p53 and Sp1 proteins, but caused G1/S delay only in normal cells. Despite the increased p53 protein, p21 did not significantly increase in NBE1 cells with overexpressed hTERT, and this correlated with the absence of G1/S delay in these cells. The data highlight the regulatory function of the XRCC4 scaffold protein and imply its connection to a transcriptional regulatory network or mRNA metabolism.
    Keywords:  NHEJ deficiency; base excision repair (BER); cell cycle; genome stability; hTERT overexpression; non-homologous end joining (NHEJ); p21 protein; scaffold protein XRCC4; transcription factor Sp1; transcription factor p53
    DOI:  https://doi.org/10.3390/ijms251910405
  32. Elife. 2024 Oct 17. pii: RP96575. [Epub ahead of print]13
      Retrotransposons (RTEs) have been postulated to reactivate with age and contribute to aging through activated innate immune response and inflammation. Here, we analyzed the relationship between RTE expression and aging using published transcriptomic and methylomic datasets of human blood. Despite no observed correlation between RTE activity and chronological age, the expression of most RTE classes and families except short interspersed nuclear elements (SINEs) correlated with biological age-associated gene signature scores. Strikingly, we found that the expression of SINEs was linked to upregulated DNA repair pathways in multiple cohorts. We also observed DNA hypomethylation with aging and the significant increase in RTE expression level in hypomethylated RTEs except for SINEs. Additionally, our single-cell transcriptomic analysis suggested a role for plasma cells in aging mediated by RTEs. Altogether, our multi-omics analysis of large human cohorts highlights the role of RTEs in biological aging and suggests possible mechanisms and cell populations for future investigations.
    Keywords:  biological aging; chronological aging; genetics; genomics; human; methylomics; retrotransposons; transcriptomics
    DOI:  https://doi.org/10.7554/eLife.96575
  33. Aging (Albany NY). 2024 Oct 17. null
      Werner syndrome of premature aging is caused by mutations in the WRN RECQ helicase/exonuclease, which functions in DNA replication, repair, transcription, and telomere maintenance. How the loss of WRN accelerates aging is not understood in full. Here we show that WRN is necessary for optimal constitutive heterochromatin levels in proliferating human fibroblasts. Locally, WRN deficiency derepresses SATII pericentromeric satellite repeats but does not reduce replication fork progression on SATII repeats. Globally, WRN loss reduces a subset of protein-protein interactions responsible for the organization of constitutive heterochromatin in the nucleus, namely, the interactions involving Lamin B1 and Lamin B receptor, LBR. Both the mRNA level and subcellular distribution of LBR are affected by WRN deficiency, and unlike the former, the latter phenotype does not require WRN catalytic activities. The phenotypes of heterochromatin disruption seen in WRN-deficient proliferating fibroblasts are also observed in WRN-proficient fibroblasts undergoing replicative or oncogene-induced senescence. WRN interacts with histone deacetylase 2, HDAC2; WRN/HDAC2 association is mediated by heterochromatin protein alpha, HP1α, and WRN complexes with HP1α and HDAC2 are downregulated in senescing cells. The data suggest that the effect of WRN loss on heterochromatin is separable from senescence program, but mimics at least some of the heterochromatin changes associated with it.
    Keywords:  Werner progeria; heterochromatin; nuclear lamina; satellite repeats; senescence
    DOI:  https://doi.org/10.18632/aging.206132
  34. Proc Natl Acad Sci U S A. 2024 Oct 22. 121(43): e2411987121
      Dietary restriction (DR) slows aging in many animals, while in some cases, the sensory signals from diet alone are sufficient to retard or accelerate lifespan. The digestive tract is a candidate location to sense nutrients, where neuropeptides secreted by enteroendocrine cells (EEC) produce systemic signals in response to food. Here, we measure how Drosophila neuropeptide F (NPF) is secreted into adult circulation by EEC and find that specific EEC differentially respond to dietary sugar and yeast. Female lifespan is increased when gut NPF is genetically depleted, and this manipulation is sufficient to blunt the longevity benefit conferred by DR. Depletion of NPF receptors at insulin-producing neurons of the brain also increases female lifespan, consistent with observations where loss of gut NPF decreases neuronal insulin secretion. The longevity conferred by repressing gut NPF and brain NPF receptors is reversed by treating adults with a juvenile hormone (JH) analog. JH is produced by the adult corpora allata, and inhibition of the insulin receptor at this tissue decreases JH titer and extends lifespan in both males and females, while this longevity is restored to wild type by treating adults with a JH analog. Overall, EEC of the gut modulate Drosophila aging through interorgan communication mediated by a gut-brain-corpora allata axis, and insulin produced in the brain impacts lifespan through its control of JH titer. These data suggest that we consider how human incretins and their analogs, which are used to treat obesity and diabetes, may impact aging.
    Keywords:  aging; incretin; insulin; interorgan communication; juvenile hormone
    DOI:  https://doi.org/10.1073/pnas.2411987121
  35. Front Pharmacol. 2024 ;15 1434024
      Organ-specific aging is increasingly recognized for its research significance, with liver aging demonstrating particular relevance due to its central role in metabolism. We have pioneered the discovery that the expression of ESRRG in the liver positively correlates with age and have established its association with clinical characteristics, including hepatic edema. Our findings link liver aging to a shift in oxidative stress states, where ESRRG, a crucial nuclear receptor responsive to oxidative stress, may be modulated by various small molecules. Through virtual screening of a natural medicinal molecule database followed by further validation, we confirmed that the natural compound Tanshinone IIA mitigates oxidative stress-induced damage in the liver via the ESRRG/Cyp2e1 pathway, thus decelerating liver aging. Importantly, our study also explores the dynamic impact of Tanshinone IIA on ESRRG conformation, providing a profound understanding of its molecular interactions with ESRRG and laying a foundation for the rational design of small molecules based on natural compounds.
    Keywords:  CYP2E1; ESRRG; Tanshinone IIA; aging; liver
    DOI:  https://doi.org/10.3389/fphar.2024.1434024
  36. Nature. 2024 Oct;634(8034): 528-531
      
    Keywords:  Immunology; Nutrition; Personalized medicine
    DOI:  https://doi.org/10.1038/d41586-024-03334-0
  37. Expert Opin Investig Drugs. 2024 Oct 16. 1-14
       INTRODUCTION: To improve kidney disease treatments, it is crucial to understand how inflammaging affects patients´ longevity. We could potentially slow down kidney disease progression and enhance longevity by targeting specific pathways involved in inflammaging with potential drugs.
    AREAS OF COVERED: This review offers an updated overview of 'anti-inflammaging' drugs currently in the kidney disease research pipeline, as well as those with potential for future therapeutic use. Furthermore, these drugs are categorized according to their mechanisms, including targeting inflammation, immune and metabolic regulation, oxidative stress, senescence, and autophagy, as demonstrated in preclinical and early clinical trials. Additionally, the review provides insights into key challenges and opinions for future advancements in this field.
    EXPERT OPINION: We reviewed recent advancements in applying different therapies to mitigate inflammaging in kidney diseases. We underscore the need for continued research to elucidate the complex pathways underlying inflammaging, which will be essential for the development of more precise and effective treatments. As research in this field advances, several emerging drugs appear promising for future investigation. While current findings are encouraging, further clinical studies are required to validate the therapeutic potential of these agents in kidney diseases, ultimately paving the way for more targeted and efficacious interventions.
    Keywords:  Autophagy; caloric restriction; inflammaging; kidney diseases; metabolic dysregulation; oxidative stress; senescence; senolytics
    DOI:  https://doi.org/10.1080/13543784.2024.2417755
  38. J Nutr. 2024 Oct 16. pii: S0022-3166(24)01094-0. [Epub ahead of print]
       BACKGROUND: NAD+ level declines with age and boosting it can improve multi-organ functions and lifespan.
    OBJECTIVE: NMN (Nicotinamide mononucleotide), a natural NAD+ (Nicotinamide adenine dinucleotide)precursor with the ability to enhance NAD+ biosynthesis. Numerous studies have shown that a high-fat diet can accelerate the process of aging and many diseases. We hypothesized that long-term administration of NMN could exert protective effects on adipose, muscle, and kidney tissues in mice on a high-fat diet act by affecting the autophagic pathway.
    METHODS: Mice at 14 months of age were fed a high-fat diet and NMN was added to their drinking water at a dose of 400 mg/kg for 7 months. The locomotor ability of the mice was assessed by behavioral experiments such as grip test, wire hang test, rotarod, and beam-walking test. At the end of the behavioral experiments, the pathological changes of each peripheral organ and the expression of autophagy-related proteins as well as the markers of the senescence and inflammaging were analyzed by pathological staining, immunohistochemical staining and western blotting, respectively.
    RESULTS: We found that NMN supplementation increased NAD+ levels and ultimately attenuated age- and diet-related physiological decline in mice. NMN inhibited high-fat-diet-induced obesity, promoted physical activity, improved glucose and lipid metabolism, improved skeletal muscle function and renal damage as well as mitigated the senescence and inflammaging as demonstrated by p16, IL-1β and TNF-α levels. In addition, the present study further emphasizes the potential mechanisms underlying the bidirectional relationship between NAD+ and autophagy. We detected changes in autophagy levels in various tissue organs, and NMN may play a protective role by inhibiting excessive autophagy induced by high-fat diet.
    CONCLUSION: Our findings demonstrated that NMN administration attenuated high fat diet-induced metabolic disorders and physiological decline in aging mice.
    Keywords:  Aging; Autophagy; High-fat diet; NAD(+); NMN; Sirtuins
    DOI:  https://doi.org/10.1016/j.tjnut.2024.10.017
  39. Int J Mol Sci. 2024 Oct 07. pii: 10773. [Epub ahead of print]25(19):
      Exercise is increasingly recognized as an effective strategy to counteract skeletal muscle aging and conditions such as sarcopenia. However, the specific exercise-induced genes responsible for these protective effects remain unclear. To address this, we conducted an eight-week aerobic exercise regimen on late-middle-aged mice and developed an integrated approach that combines mouse exercise-induced genes with human GWAS datasets to identify causal genes for sarcopenia. This approach led to significant improvements in the skeletal muscle phenotype of the mice and the identification of exercise-induced genes and miRNAs. By constructing a miRNA regulatory network enriched with transcription factors and GWAS signals related to muscle function and traits, we focused on 896 exercise-induced genes. Using human skeletal muscle cis-eQTLs as instrumental variables, 250 of these exercise-induced genes underwent two-sample Mendelian randomization analysis, identifying 40, 68, and 62 causal genes associated with sarcopenia and its clinical indicators-appendicular lean mass (ALM) and hand grip strength (HGS), respectively. Sensitivity analyses and cross-phenotype validation confirmed the robustness of our findings. Consistently across the three outcomes, RXRA, MDM1, RBL2, KCNJ2, and ADHFE1 were identified as risk factors, while NMB, TECPR2, MGAT3, ECHDC2, and GINM1 were identified as protective factors, all with potential as biomarkers for sarcopenia progression. Biological activity and disease association analyses suggested that exercise exerts its anti-sarcopenia effects primarily through the regulation of fatty acid oxidation. Based on available drug-gene interaction data, 21 of the causal genes are druggable, offering potential therapeutic targets. Our findings highlight key genes and molecular pathways potentially responsible for the anti-sarcopenia benefits of exercise, offering insights into future therapeutic strategies that could mimic the safe and mild protective effects of exercise on age-related skeletal muscle degeneration.
    Keywords:  exercise; sarcopenia; skeletal muscle aging; transcriptome; two-sample Mendelian randomization
    DOI:  https://doi.org/10.3390/ijms251910773
  40. bioRxiv. 2024 Oct 13. pii: 2024.10.09.617512. [Epub ahead of print]
      Biological age estimation from DNA methylation and determination of relevant biomarkers is an active research problem which has predominantly been tackled with black-box penalized regression. Machine learning is used to select a small subset of features from hundreds of thousands CpG probes and to increase generalizability typically lacking with ordinary least-squares regression. Here, we show that such feature selection lacks biological interpretability and relevance in the clocks of the first- and next-generations, and clarify the logic by which these clocks systematically exclude biomarkers of aging and disease. Moreover, in contrast to the assumption that regularized linear regression is needed to prevent overfitting, we demonstrate that hypothesis-driven selection of biologically relevant features in conjunction with ordinary least squares regression yields accurate, well-calibrated, generalizable clocks with high interpretability. We further demonstrate that the interplay of disease-related shifts of predictor values and their corresponding weights, which we term feature shifts, contributes to the lack of resolution between health and disease in conventional linear models. Lastly, we introduce a method of feature rectification, which aligns these shifts to improve the distinction of age predictions for healthy people vs. patients with various diseases.
    Key Findings: There is no apparent biological significance of the CpGs selected by first- and next-generation clocksThe range of residuals for first- and next-generation clock predications on healthy samples is very large; for all models tested, a prediction error of +/-10-20 years is within the 95% range of variation for healthy controls and does not signify age accelerationThere is no significant shift in the mean of residuals for patient populations relative to healthy populations for most studied first- and next-generation clocks. For those with significance, the effect size is very small.Hypothesis-driven feature pre-selection, coupled with modified forward step-wise selection yields age predictors on par with first and next-generation clocks. EN/ML is not needed.Disease-related shifts at different CpG probes, along with learned model weights, can be either positive or negative; their combination leads to de-coherence effect in linear models.Model coherence can be induced by rectifying features to have only positive shifts in patient samples; this provides a better resolution between health and disease in DNAm age models, and expectedly, introduces more non-linearity to the input data.
    DOI:  https://doi.org/10.1101/2024.10.09.617512
  41. Nat Commun. 2024 Oct 19. 15(1): 9030
      While previous studies identified common genetic variants associated with longevity in centenarians, the role of the rare loss-of-function (LOF) mutation burden remains largely unexplored. Here, we investigated the burden of rare LOF mutations in Ashkenazi Jewish individuals from the Longevity Genes Project and LonGenity study cohorts using whole-exome sequencing data. We found that centenarians had a significantly lower burden (11-22%) of LOF mutations compared to controls. Similar effects were also observed in their offspring. Gene-level burden analysis identified 35 genes with depleted LOF mutations in centenarians, with 14 of these validated in the UK Biobank. Mendelian randomization and multi-omic analyses on these genes identified RGP1, PCNX2, and ANO9 as longevity genes with consistent causal effects on multiple aging-related traits and altered expression during aging. Our findings suggest that a protective genetic background, characterized by a reduced burden of damaging variants, contributes to exceptional longevity, likely acting in concert with specific protective variants to promote healthy aging.
    DOI:  https://doi.org/10.1038/s41467-024-52967-2
  42. Proc Natl Acad Sci U S A. 2024 Oct 22. 121(43): e2403906121
      The conserved mesencephalic astrocyte-derived neurotrophic factor (MANF) is known for protecting dopaminergic neurons and functioning in various other tissues. Previously, we showed that Caenorhabditis elegans manf-1 null mutants exhibit defects such as increased endoplasmic reticulum (ER) stress, dopaminergic neurodegeneration, and abnormal protein aggregation. These findings suggest an essential role for MANF in cellular processes. However, the mechanisms by which intracellular and extracellular MANF regulate broader cellular functions remain unclear. We report a unique mechanism of action for MANF-1 that involves the transcription factor HLH-30/TFEB-mediated signaling to regulate autophagy and lysosomal function. Multiple transgenic strains overexpressing MANF-1 showed extended lifespan of animals, reduced protein aggregation, and improved neuronal survival. Using fluorescently tagged MANF-1, we observed tissue-specific localization of the protein, which was dependent on the ER retention signal. Further subcellular analysis showed that MANF-1 localizes within cells to the lysosomes and utilizes the endosomal pathway. Consistent with the lysosomal localization, our transcriptomic study of MANF-1 and analyses of autophagy regulators demonstrated that MANF-1 promotes proteostasis by regulating autophagic flux and lysosomal activity. Collectively, our findings establish MANF as a critical regulator of stress response, proteostasis, and aging.
    Keywords:  ER stress; MANF-1; longevity; nematode; proteostasis
    DOI:  https://doi.org/10.1073/pnas.2403906121
  43. Sci Rep. 2024 10 16. 14(1): 24238
      Deoxyribonucleic acid (DNA) is able to form non-canonical four-stranded helical structures with diverse folding patterns known as G-quadruplexes (G4s). G4 topologies are classified based on their relative strand orientation following the 5' to 3' phosphate backbone polarity. Broadly, G4 topologies are either parallel (4+0), antiparallel (2+2), or hybrid (3+1). G4s play crucial roles in biological processes such as DNA repair, DNA replication, transcription and have thus emerged as biological targets in drug design. While computational models have been developed to predict G4 formation, there is currently no existing model capable of predicting G4 folding topology based on its nucleic acid sequence. Therefore, we introduce G4ShapePredictor (G4SP), an application featuring a collection of multi-classification machine learning models that are trained on a custom G4 dataset combining entries from existing literature and in-house circular dichroism experiments. G4ShapePredictor is designed to accurately predict G4 folding topologies in potassium ( K+ ) buffer based on its primary sequence and is able to incorporate a threshold optimization strategy allowing users to maximise precision. Furthermore, we have identified three topological sequence motifs that suggest specific G4 folding topologies of (4+0), (2+2) or (3+1) when utilising the decision-making mechanisms of G4ShapePredictor.
    DOI:  https://doi.org/10.1038/s41598-024-74826-2
  44. Ageing Res Rev. 2024 Oct 10. pii: S1568-1637(24)00357-X. [Epub ahead of print] 102539
      Retrotransposons are self-replicating genomic elements that move from one genomic location to another using a "copy-and-paste" method involving RNA intermediaries. One family of retrotransposon that has garnered considerable attention for its association with age-related diseases and anti-aging interventions is the short interspersed nuclear elements (SINEs). This review summarizes current knowledge on the roles of SINEs in aging processes and therapies. To underscore the significant research on the involvement of SINEs in aging-related diseases, we commence by outlining compelling evidence on the classification and mechanism, highlighting implications in age-related phenomena. The intricate relationship between SINEs and diseases such as neurodegenerative disorders, heart failure, high blood pressure, atherosclerosis, type 2 diabetes mellitus, osteoporosis, visual system dysfunctions, and cancer is explored, emphasizing their roles in various age-related diseases. Recent investigations into the anti-aging potential of SINE-targeted treatments are examined, with particular attention to how SINE antisense RNA mitigate age-related alterations at the cellular and molecular levels, offering insights into potential therapeutic targets for age-related pathologies. This review aims to compile the most recent advances on the multifaceted roles of SINE retrotransposons in age-related diseases and anti-aging interventions, providing valuable insights into underlying mechanisms and therapeutic avenues for promoting healthy aging.
    Keywords:  Age-related diseases; Alu; Anti-aging activity; Retrotransposable elements; SINEs
    DOI:  https://doi.org/10.1016/j.arr.2024.102539
  45. Cell Death Discov. 2024 Oct 13. 10(1): 436
      Polyploidy is frequently enhanced under pathological conditions, such as tissue injury and cancer in humans. Polyploidization is critically involved in cancer evolution, including cancer initiation and the acquisition of drug resistance. However, the effect of polyploidy on cell fate remains unclear. In this study, we explored the effects of polyploidization on cellular responses to DNA damage and cell cycle progression. Through various comparisons based on ploidy stratifications of cultured cells, we found that polyploidization and the accumulation of genomic DNA damage mutually induce each other, resulting in polyploid cells consistently containing more genomic DNA damage than diploid cells under both physiological and stress conditions. Notably, despite substantial DNA damage, polyploid cells demonstrated a higher tolerance to its impact, exhibiting delayed cell cycle arrest and reduced secretion of inflammatory cytokines associated with DNA damage-induced senescence. Consistently, in mice with ploidy tracing, hepatocytes with high ploidy appeared to potentially persist in the damaged liver, while being susceptible to DNA damage. Polyploidy acts as a reservoir of genomic damage by mitigating the impact of DNA damage, while simultaneously enhancing its accumulation.
    DOI:  https://doi.org/10.1038/s41420-024-02206-w
  46. Nutrients. 2024 Sep 27. pii: 3271. [Epub ahead of print]16(19):
       BACKGROUND: Sarcopenia is characterized by the progressive loss of skeletal muscle mass, strength, and function, significantly impacting overall health and quality of life in older adults. This narrative review explores emerging targets and potential treatments for sarcopenia, aiming to provide a comprehensive overview of current and prospective interventions.
    METHODS: The review synthesizes current literature on sarcopenia treatment, focusing on recent advancements in muscle regeneration, mitochondrial function, nutritional strategies, and the muscle-microbiome axis. Additionally, pharmacological and lifestyle interventions targeting anabolic resistance and neuromuscular junction integrity are discussed.
    RESULTS: Resistance training and adequate protein intake remain the cornerstone of sarcopenia management. Emerging strategies include targeting muscle regeneration through myosatellite cell activation, signaling pathways, and chronic inflammation control. Gene editing, stem cell therapy, and microRNA modulation show promise in enhancing muscle repair. Addressing mitochondrial dysfunction through interventions aimed at improving biogenesis, ATP production, and reducing oxidative stress is also highlighted. Nutritional strategies such as leucine supplementation and anti-inflammatory nutrients, along with dietary modifications and probiotics targeting the muscle-microbiome interplay, are discussed as potential treatment options. Hydration and muscle-water balance are emphasized as critical in maintaining muscle health in older adults.
    CONCLUSIONS: A combination of resistance training, nutrition, and emerging therapeutic interventions holds potential to significantly improve muscle function and overall health in the aging population. This review provides a detailed exploration of both established and novel approaches for the prevention and management of sarcopenia, highlighting the need for further research to optimize these strategies.
    Keywords:  hydration; inflammaging; mitochondrial dysfunction; muscle health; neuromuscular junction; physical performance; satellite cells
    DOI:  https://doi.org/10.3390/nu16193271
  47. J Neuroinflammation. 2024 Oct 12. 21(1): 260
      Haploinsufficiency of the transcriptional repressor ZBTB18/RP58 is associated with intellectual disability. However, the mechanisms causing this disability are unknown, and preventative measures and treatments are not available. Here, we assessed multiple behaviors in Zbtb18/Rp58 heterozygous-knockout mice, and examined local field potentials, DNA fragmentation, mitochondrial morphology, and performed histochemical and transcriptome analyses in the hippocampus to evaluate chronic inflammation. In wild-type mice, object location memory was present at a similar level at 2 and 4-5 months of age, and became impaired at 12-18 months. In contrast, Zbtb18/Rp58 heterozygous-knockout mice displayed early onset impairments in object location memory by 4-5 months of age. These mice also exhibited earlier accumulation of DNA and mitochondrial damage, and activated microglia in the dentate gyrus, which are associated with defective DNA repair. Notably, chronic minocycline therapy, which has neuroprotective and anti-inflammatory effects, attenuated age-related phenotypes, including accumulation of DNA damage, increased microglial activation, and impairment of object location memory. Our results suggest that Zbtb18/Rp58 activity is required for DNA repair and its reduction results in DNA and mitochondrial damage, increased activation of microglia, and inflammation, leading to accelerated declines in cognitive functions. Minocycline has potential as a therapeutic agent for the treatment of ZBTB18/RP58 haploinsufficiency-associated cognitive dysfunction.
    Keywords:  Cognitive decline; DNA damage; DNA repair; Inflammation; Intellectual disability; ZBTB18/RP58
    DOI:  https://doi.org/10.1186/s12974-024-03217-1
  48. Ageing Res Rev. 2024 Oct 10. pii: S1568-1637(24)00358-1. [Epub ahead of print] 102540
      Age-related changes initiate a cascade of cellular and molecular alterations that lead to immune system dysfunction or abnormal activation, predisposing individuals to age-related diseases. This phenomenon, commonly referred to as immunosenescence, highlighting aging-associated progressive decline of the immune system. Moreover, mounting evidence suggests that immunosenescence contributes to a related pathological phenomenon known as inflammaging. Inflammaging refers to chronic, low-grade, and systemic inflammation associated with aging, occurring despite the absence of overt stimuli. In the body, inflammation is typically activated in response to overt stimuli such as bacterial/microbial invasion or a pathological state, however, inflammaging occurrence and its underpinning mechansisms seem to be independent and in the absence of such stimuli. Despite recent advancements in molecular characterization and the scrutiny of disease relevance, these two interconnected concepts have remained largely unexplored and unrecognized. In this comprehensive review, we aim to shed light on the mechanistic and cellular aspects of immunosenescence and inflammaging, as well as their pivotal roles in the pathogenesis of aging-related diseases, including cancer, infections, dementia, and neurodegenerative disorders.
    Keywords:  Immunosenescence; Inflammaging; Inflammation; aging; cancer; dementia; infections; neurodegeneration
    DOI:  https://doi.org/10.1016/j.arr.2024.102540
  49. Nat Biotechnol. 2024 Oct 16.
      Lipid nanoparticle (LNP) delivery of clustered regularly interspaced short palindromic repeat (CRISPR) ribonucleoproteins (RNPs) could enable high-efficiency, low-toxicity and scalable in vivo genome editing if efficacious RNP-LNP complexes can be reliably produced. Here we engineer a thermostable Cas9 from Geobacillus stearothermophilus (GeoCas9) to generate iGeoCas9 variants capable of >100× more genome editing of cells and organs compared with the native GeoCas9 enzyme. Furthermore, iGeoCas9 RNP-LNP complexes edit a variety of cell types and induce homology-directed repair in cells receiving codelivered single-stranded DNA templates. Using tissue-selective LNP formulations, we observe genome-editing levels of 16‒37% in the liver and lungs of reporter mice that receive single intravenous injections of iGeoCas9 RNP-LNPs. In addition, iGeoCas9 RNPs complexed to biodegradable LNPs edit the disease-causing SFTPC gene in lung tissue with 19% average efficiency, representing a major improvement over genome-editing levels observed previously using viral or nonviral delivery strategies. These results show that thermostable Cas9 RNP-LNP complexes can expand the therapeutic potential of genome editing.
    DOI:  https://doi.org/10.1038/s41587-024-02437-3
  50. Anal Chem. 2024 Oct 16.
      Mitochondrial DNA G-quadruplexes (mtDNA G4s) play potential regulatory roles in mitochondrial functions. Fluorescent probes for imaging mtDNA G4s may provide useful information to unveil their regulating dynamics and functions. However, the existing probes for mtDNA G4s still exhibit short absorption and emission wavelengths and limited sensitivity. Here, we develop a new isaindigotone-derived near-infrared (NIR) fluorogenic probe for imaging mtDNA G4s in live cells and in vivo. Different fluorescent probes are engineered by conjugating the isaindigotone scaffold with varying electron-donating groups. It is shown that the probe ISAP using dimethylaminophenyl as the electron-donating group exhibits near-infrared absorption/emission and a high fluorescence activation fold in response to G4s. Molecular docking simulations reveal that ISAP binds to c-Myc G4 via multiple π-π stacking and hydrogen-bond interaction. Cellular studies show that ISAP exhibits an excellent mitochondrial targeting ability and allows specific imaging of mtDNA G4s. We further employed ISAP to image the dynamics of mtDNA G4s under glycolysis and oxidative stresses in live cells. Its capability to mtDNA G4s in vivo is showcased using a tumor-bearing mice model. This probe may serve as a useful tool to image mtDNA G4s and interrogate their biological roles in living systems.
    DOI:  https://doi.org/10.1021/acs.analchem.4c03722
  51. Int J Mol Med. 2024 Dec;pii: 117. [Epub ahead of print]54(6):
      Hypoxic ischemia is the primary cause of brain damage in newborns. Notably, copper supplementation has potential benefits in ischemic brain damage; however, the precise mechanisms underlying this protective effect remain unclear. In the present study, a hypoxic HT22 cell model was developed to examine the mechanism by which copper mitigates hypoxia‑induced oxidative stress. Cell viability was assessed using the Cell Counting Kit‑8 assay, mitochondrial structure was examined with a transmission electron microscope, intracellular ferrous ions and lipid reactive oxygen species levels in HT22 cells were measured using FerroOrange and BODIPY 581/591 C11 staining, copper content was determined using graphite furnace atomic absorption spectroscopy, and gene and protein expression were analyzed by reverse transcription‑quantitative PCR and western blotting. The present findings indicated that hypoxic exposure may lead to reduced cell viability, along with the upregulation of various markers associated with ferroptosis. Furthermore, hypoxia elevated the levels of reactive oxygen species, hydrogen peroxide and malondialdehyde, and decreased the activity of superoxide dismutase 1 (SOD1) in HT22 cells. In addition, the intracellular copper concentration exhibited a notable decrease, while supplementation with an appropriate dose of copper effectively shielded neurons from hypoxia‑induced oxidative stress and ferroptosis, and elevated cell viability in hypoxia‑exposed HT22 cells through the copper chaperone for superoxide dismutase/SOD1/glutathione peroxidase 4 axis. In conclusion, the present study identified a novel function of copper in protecting neurons from oxidative stress and ferroptosis under hypoxic conditions, providing fresh insights into the therapeutic potential of copper in mitigating hypoxia‑induced neuronal injury.
    Keywords:  copper; ferroptosis; hypoxia; neurons; oxidative stress
    DOI:  https://doi.org/10.3892/ijmm.2024.5441
  52. bioRxiv. 2024 Oct 14. pii: 2024.10.08.617286. [Epub ahead of print]
    Dog Aging Project Consortium
      Within a species, larger individuals often have shorter lives and higher rates of age-related disease. Despite this well-known link, we still know little about underlying age-related epigenetic differences, which could help us better understand inter-individual variation in aging and the etiology, onset, and progression of age-associated disease. Dogs exhibit this negative correlation between size, health, and longevity and thus represent an excellent system in which to test the underlying mechanisms. Here, we quantified genome-wide DNA methylation in a cohort of 864 dogs in the Dog Aging Project. Age strongly patterned the dog epigenome, with the majority (66% of age-associated loci) of regions associating age-related loss of methylation. These age effects were non-randomly distributed in the genome and differed depending on genomic context. We found the LINE1 (long interspersed elements) class of TEs (transposable elements) were the most frequently hypomethylated with age (FDR < 0.05, 40% of all LINE1 regions). This LINE1 pattern differed in magnitude across breeds of different sizes- the largest dogs lost 0.26% more LINE1 methylation per year than the smallest dogs. This suggests that epigenetic regulation of TEs, particularly LINE1s, may contribute to accelerated age and disease phenotypes within a species. Since our study focused on the methylome of immune cells, we looked at LINE1 methylation changes in golden retrievers, a breed highly susceptible to hematopoietic cancers, and found they have accelerated age-related LINE1 hypomethylation compared to other breeds. We also found many of the LINE1s hypomethylated with age are located on the X chromosome and are, when considering X chromosome inactivation, counter-intuitively more methylated in males. These results have revealed the demethylation of LINE1 transposons as a potential driver of inter-species, demographic-dependent aging variation.
    DOI:  https://doi.org/10.1101/2024.10.08.617286
  53. Sci Rep. 2024 10 15. 14(1): 24185
      The primary role of telomerase is the lengthening of telomeres. Nonetheless, emerging evidence highlights additional functions of telomerase outside of the nucleus. Specifically, its catalytic subunit, TERT (Telomerase Reverse Transcriptase), is detected in the cytosol and mitochondria. Several studies have suggested an elevation in TERT concentration within mitochondria in response to oxidative stress. However, the origin of this mitochondrial TERT, whether transported from the nucleus or synthesized de novo, remains uncertain. In this study, we investigate the redistribution of TERT, labeled with a SNAP-tag, in response to oxidative stress using laser scanning fluorescence microscopy. Our findings reveal that, under our experimental conditions, there is no discernible transport of TERT from the nucleus to the mitochondria due to oxidative stress.
    Keywords:  Mitochondria; Oxidative stress; Protein transport; SNAP-tag; TERT
    DOI:  https://doi.org/10.1038/s41598-024-75127-4
  54. Cell Rep. 2024 Oct 16. pii: S2211-1247(24)01240-3. [Epub ahead of print]43(11): 114889
      The special AT-rich sequence-binding (SATB) protein DVE-1 is widely recognized for its pivotal involvement in orchestrating the retrograde mitochondrial unfolded protein response (mitoUPR) in C. elegans. In our study of downstream factors contributing to lifespan extension in sensory ciliary mutants, we find that DVE-1 is crucial for this longevity effect independent of its canonical mitoUPR function. Additionally, DVE-1 also influences lifespan under conditions of dietary restriction and germline loss, again distinct from its role in mitoUPR. Mechanistically, while mitochondrial stress typically prompts nuclear accumulation of DVE-1 to initiate the transcriptional mitoUPR program, these long-lived mutants reduce DVE-1 nuclear accumulation, likely by enhancing its cytosolic translocation. This observation suggests a cytosolic role for DVE-1 in lifespan extension. Overall, our study implies that, in contrast to the more narrowly defined role of the mitoUPR-related transcription factor ATFS-1, DVE-1 may possess broader functions than previously recognized in modulating longevity and defending against stress.
    Keywords:  ATFS-1; C. elegans; CP: Cell biology; CP: Molecular biology; DVE-1; cilia; dietary restriction; germline signaling; longevity; mitoUPR
    DOI:  https://doi.org/10.1016/j.celrep.2024.114889
  55. Mol Cell Biol. 2024 Oct 10. 1-15
      The CK1 family are conserved serine/threonine kinases with numerous substrates and cellular functions. The fission yeast CK1 orthologues Hhp1 and Hhp2 were first characterized as regulators of DNA repair, but the mechanism(s) by which CK1 activity promotes DNA repair had not been investigated. Here, we found that deleting Hhp1 and Hhp2 or inhibiting CK1 catalytic activities in yeast or in human cells increased double-strand breaks (DSBs). The primary pathways to repair DSBs, homologous recombination and nonhomologous end joining, were both less efficient in cells lacking Hhp1 and Hhp2 activity. To understand how Hhp1 and Hhp2 promote DNA damage repair, we identified new substrates of these enzymes using quantitative phosphoproteomics. We confirmed that Arp8, a component of the INO80 chromatin remodeling complex, is a bona fide substrate of Hhp1 and Hhp2 important for DNA repair. Our data suggest that Hhp1 and Hhp2 facilitate DNA repair by phosphorylating multiple substrates, including Arp8.
    Keywords:  Arp8; CK1, casein kinase 1; DNA repair; INO80; Schizosaccharomyces pombe; homologous recombination; nonhomologous end joining; phosphoproteomics
    DOI:  https://doi.org/10.1080/10985549.2024.2408016
  56. Cell Commun Signal. 2024 Oct 14. 22(1): 495
      The DNA damage response is a highly conserved protective mechanism that enables cells to cope with various lesions in the genome. Extensive studies across different eukaryotic cells have identified the crucial roles played by components required for response to DNA damage. When compared to the essential signal transducers and repair factors in the DNA damage response circuitry, the negative regulators and underlying mechanisms of this circuitry have been relatively under-examined. In this study, we investigated Gst1, a putative glutathione transferase in the fungal pathogen Candida albicans. We found that under stress caused by the DNA damage agent MMS, GST1 expression was significantly upregulated, and this upregulation was further enhanced by the loss of the checkpoint kinases and DNA repair factors. Somewhat counterintuitively, deletion of GST1 conferred increased resistance to MMS, potentially via enhancing the phosphorylation of Rad53. Furthermore, overexpression of RAD53 or deletion of GST1 resulted in upregulated transcription of DNA damage repair genes, including CAS1, RAD7, and RAD30, while repression of RAD7 transcription in the GST1 deletion reversed the strain's heightened resistance to MMS. Finally, Gst1 physically interacted with Rad53, and their interaction weakened in response to MMS-induced stress. Overall, our findings suggest a negative regulatory role for GST1 in DNA damage response in C. albicans, and position Gst1 within the Rad53-mediated signaling pathway. These findings hold significant implications for understanding the mechanisms underlying the DNA damage response in this fungal pathogen and supply new potential targets for therapeutic intervention.
    Keywords:   Candida albicans ; DNA damage response; Glutathione transferase; Gst1; Rad53
    DOI:  https://doi.org/10.1186/s12964-024-01865-7
  57. Immunol Rev. 2024 Oct 17.
      The NLRP3 inflammasome is a multiprotein complex that upon activation by the innate immune system drives a broad inflammatory response. The primary initial mediators of this response are pro-IL-1β and pro-IL-18, both of which are in an inactive form. Formation and activation of the NLRP3 inflammasome activates caspase-1, which cleaves pro-IL-1β and pro-IL-18 and triggers the formation of gasdermin D pores. Gasdermin D pores allow for the secretion of active IL-1β and IL-18 initiating the organism-wide inflammatory response. The NLRP3 inflammasome response can be beneficial to the host; however, if the NLRP3 inflammasome is inappropriately activated it can lead to significant pathology. While the primary components of the NLRP3 inflammasome are known, the precise details of assembly and activation are less well defined and conflicting. Here, we discuss several of the proposed pathways of activation of the NLRP3 inflammasome. We examine the role of subcellular localization and the reciprocal regulation of the NLRP3 inflammasome by autophagy. We focus on the roles of mitochondria and mitophagy in activating and regulating the NLRP3 inflammasome. Finally, we detail the impact of pathologic NLRP3 responses in the development and manifestations of pulmonary disease.
    Keywords:  NLRP3; caspase‐1; inflammasome; lung injury; mitochondria
    DOI:  https://doi.org/10.1111/imr.13410
  58. Biomater Sci. 2024 Oct 17.
      Various factors can contribute to bone damage or loss, presenting challenges for bone regeneration. Our study explores the potential clinical applications of two processed forms of Wharton's jelly of the human umbilical cord for treating bone loss. Wharton's jelly from fresh umbilical cords underwent two distinct processes: (1) frozen Wharton's jelly (WJF), preserved with cryoprotective agents, and (2) decellularized Wharton's jelly matrix (WJD), prepared only via lyophilization without cryoprotectants. Both WJD and WJF are rich in collagen, hyaluronan, and polysaccharide proteins. Notably, WJD exhibited a porous structure lacking nuclei from human umbilical cord mesenchymal stem cells, unlike WJF. In direct contact experiments, WJD stimulated osteoblast migration, enhanced osteoblast maturation, and promoted calcium deposition for bone formation when administered to cultured rat osteoblasts. Furthermore, in transwell co-culture experiments, both WJD and WJF increased the rat osteoblast expression of RUNX2 and OPN genes, elevated alkaline phosphatase levels, and enhanced extracellular calcium precipitation, indicating their role in osteoblast maturation and new bone formation. Hyaluronic acid, one of the ingredients from WJD and WJF, was identified as a key component triggering osteogenesis. In vivo experiments involved creating circular bone defects in the calvarias of rats, where WJD and WJF were separately implanted and monitored over five months using micro-computerized tomography. Our results demonstrated that both WJD and WJF enhanced angiogenesis, collagen formation, osteoblast maturation, and bone growth within the bone defects. In summary, WJD and WJF, natural biomaterials with biocompatibility and nontoxicity, act not only as effective scaffolds but also promote osteoblast adhesion and differentiation, and accelerate osteogenesis.
    DOI:  https://doi.org/10.1039/d3bm02137h
  59. bioRxiv. 2024 Oct 13. pii: 2024.10.11.617885. [Epub ahead of print]
      Diminished signaling via insulin/insulin-like growth factor-1 (IGF-1) axis is associated with longevity in different model organisms. IGF-1 gene is highly conserved across species, with only few evolutionary changes identified in it. Despite its potential role in regulating life span, no coding variants in IGF-1 have been reported in human longevity cohorts to date. This study investigated the whole exome sequencing data from 2,487 individuals in a cohort of Ashkenazi Jewish centenarians, their offspring, and controls without familial longevity to identify functional IGF-1 coding variants. We identified two likely functional coding variants IGF-1 :p.Ile91Leu and IGF-1 :p.Ala118Thr in our longevity cohort. Notably, a centenarian specific novel variant IGF-1:p .Ile91Leu was located at the binding interface of IGF-1 - IGF-1R, whereas IGF-1 :p.Ala118Thr was significantly associated with lower circulating levels of IGF-1. We performed extended all-atom molecular dynamics simulations to evaluate the impact of Ile91Leu on stability, binding dynamics and energetics of IGF-1 bound to IGF-1R. The IGF-1 :p.Ile91Leu formed less stable interactions with IGF-1R's critical binding pocket residues and demonstrated lower binding affinity at the extracellular binding site compared to wild-type IGF-1. Our findings suggest that IGF-1 :p.Ile91Leu and IGF-1 :p.Ala118Thr variants attenuate IGF-1R activity by impairing IGF-1 binding and diminishing the circulatory levels of IGF-1, respectively. Consequently, diminished IGF-1 signaling resulting from these variants may contribute to exceptional longevity in humans.
    DOI:  https://doi.org/10.1101/2024.10.11.617885
  60. Ter Arkh. 2024 Sep 14. 96(8): 826-835
      Ferritin, an iron transport protein, is an acute phase protein of inflammation and oxidative stress (OS), a biomarker of cytolysis and ferroptosis. Inflammation, OS and iron overload are characteristic processes of the pathophysiology of aging. Human placental hydrolysates (HPHs) are promising hepatoprotective agents for anti-aging therapy. The goal of the team of authors was to systematize data on ferritin as a marker of aging and to identify peptides that counteract the aging pathophysiology, including through the regulation of iron and ferritin metabolism, in the HPH Laennec (manufactured by Japan Bioproducts). The results of basic and clinical studies confirm the above relationships and indicate that blood ferritin levels characterize the chronological and biological aging of the human body.
    Keywords:  aging; ferritin; ferroptosis; inflammation; iron overload; proteomics
    DOI:  https://doi.org/10.26442/00403660.2024.08.202811
  61. bioRxiv. 2024 Oct 13. pii: 2024.10.11.617852. [Epub ahead of print]
      Hippo-YAP signaling orchestrates epithelial tissue repair and is therefore an attractive target in regenerative medicine. Yet it is unresolved how YAP controls the underlying transient proliferative response. Here we show that YAP-TEAD activation increases the nuclear cyclin D1/p27 protein ratio in G1 phase, towards a threshold level that dictates whether individual cells enter or exit the cell cycle. YAP increases this ratio indirectly, by increasing EGFR and other receptor activities that signal primarily through ERK. Conversely, contact inhibition suppresses YAP activity which gradually downregulates mitogen signaling and the cyclin D1/p27 ratio. Increasing YAP activity by ablating the suppressor Merlin/NF2 reveals a robust balancing mechanism in which YAP can still be inhibited after cell division further increases local cell density. Thus, critical for tissue repair, the proliferation response is intrinsically transient since the YAP-induced and mitogen-mediated increase in the cyclin D1/p27 ratio is reliably reversed through delayed contact inhibition of YAP.
    HIGHLIGHTS: YAP signaling controls cell cycle entry and exit by up- and down-regulating the cyclin D1/p27 ratio above and below a conserved thresholdYAP-induced proliferation is intrinsically transient since contact inhibition of YAP suppresses EGFR signaling after a delay to reduce this cyclin D1/p27 ratioYAP can still be robustly inhibited after Merlin/NF2 ablation but only at higher local cell densityThe YAP-regulated cyclin D1/p27 ratio is primarily controlled by MEK-ERK rather than mTOR activity.
    DOI:  https://doi.org/10.1101/2024.10.11.617852
  62. Cell Oncol (Dordr). 2024 Oct 16.
       PURPOSE: Autophagy is frequently observed in tissues during the aging process, yet the tissues most strongly correlated with autophagy during aging and the underlying regulatory mechanisms remain inadequately understood. The purpose of this study is to identify the tissues with the highest correlation between autophagy and aging, and to explore the functions and mechanisms of autophagy in the aging tissue microenvironment.
    METHODS: Integrated bulk RNA-seq from over 7000 normal tissue samples, single-cell sequencing data from blood samples of different ages, more than 2000 acute myeloid leukemia (AML) bulk RNA-seq, and multiple sets of AML single-cell data. The datasets were analysed using various bioinformatic approaches.
    RESULTS: Blood tissue exhibited the highest positive correlation between autophagy and aging among healthy tissues. Single-cell resolution analysis revealed that in aged blood, classical monocytes (C. monocytes) are most closely associated with elevated autophagy levels. Increased autophagy in these monocytes correlated with a higher proportion of C. monocytes, with hypoxia identified as a crucial contributing factor. In AML, a representative myeloid blood disease, enhanced autophagy was accompanied by an increased proportionof C. monocytes. High autophagy levels in monocytes are associated with pro-inflammatory gene upregulation and Reactive Oxygen Species (ROS) accumulation, contributing to tissue aging.
    CONCLUSION: This study revealed that autophagy is most strongly correlated with aging in blood tissue. Enhanced autophagy levels in C. monocytes demonstrate a positive correlation with increased secretion of pro-inflammatory factors and elevated production of ROS, which may contribute to a more rapid aging process. This discovery underscores the critical role of autophagy in blood aging and suggests potential therapeutic targets to mitigate aging-related health issues.
    Keywords:  Aging; Autophagy; Hypoxia; Monocytes; Reactive oxygen species
    DOI:  https://doi.org/10.1007/s13402-024-00996-w
  63. bioRxiv. 2024 Oct 13. pii: 2024.10.12.618004. [Epub ahead of print]
      Age-related inflammation or inflammaging is a key mechanism that increases disease burden and may control lifespan. How adipose tissue macrophages (ATMs) control inflammaging is not well understood in part because the molecular identities of niche-specific ATMs are incompletely known. Using intravascular labeling to exclude circulating myeloid cells and subsequent single-cell sequencing with orthogonal validation, we define the diversity and alterations in niche resident ATMs through lifespan. Aging led to depletion of vessel-associated macrophages (VAMs), expansion of lipid-associated macrophages (LAMs), and emergence of a unique subset of CD38+ age-associated macrophages (AAMs) in visceral white adipose tissue (VAT). Interestingly, CD169+CD11c- ATMs are enriched in a subpopulation of nerve-associated macrophages (NAMs) that declines with age. Depletion of CD169+ NAMs in aged mice increases inflammaging and impairs lipolysis suggesting that they are necessary for preventing catecholamine resistance in VAT. These findings reveal specialized ATMs control adipose homeostasis and link inflammation to tissue dysfunction during aging.
    DOI:  https://doi.org/10.1101/2024.10.12.618004