bims-longev Biomed News
on Longevity
Issue of 2023–01–29
eightteen papers selected by
Andreea Nitescu
  1. Oxidative stress, inflammation and hormesis: The role of dietary and lifestyle modifications on aging.
  2. Emerging Nutrition Approaches to Support the Mind and Muscle for Healthy Aging.
  3. Editorial: Somatic mutations, genome mosaicism and aging.
  4. Can Brain-Derived Neurotrophic Factor (Bdnf) Mimetics Be A Way Out For Neurodegenerative Diseases?
  5. Autophagy as an Anti-senescent in Aging Neurocytes.
  6. Are menopause, aging and prostate cancer diseases?
  7. Targeting senescent cells for a healthier longevity: the roadmap for an era of global aging.
  8. How does apolipoprotein E genotype influence the relationship between physical activity and Alzheimer's disease risk? A novel integrative model.
  9. Mechanisms of action of vitamin D in delaying aging and preventing disease by inhibiting oxidative stress.
  10. Insights on the role of L-lactate as a signaling molecule in skin aging.
  11. Mechanism of action and therapeutic effects of oxidative stress and stem cell-based materials in skin aging: Current evidence and future perspectives.
  12. Defective proteostasis in Alzheimer's disease.
  13. Gut-derived β-amyloid: Likely a centerpiece of the gut-brain axis contributing to Alzheimer's pathogenesis.
  14. Investigation of genetic variants and causal biomarkers associated with brain aging.
  15. Are Alzheimer's and coronary artery diseases genetically related to longevity?
  16. Unveiling new secrets in Parkinson's disease: the glycatome.
  17. Mulberroside A alleviates osteoarthritis via restoring impaired autophagy and suppressing MAPK/NF-κB/PI3K-AKT-mTOR signaling pathways.
  18. The association between sleep quality and telomere length: A systematic literature review.
  1. Neurochem Int. 2023 Jan 23. pii: S0197-0186(23)00018-9. [Epub ahead of print] 105490
    Oxidative stress, inflammation and hormesis: The role of dietary and lifestyle modifications on aging.
    Vinita Sharma, Mohammad Murtaza Mehdi.
      Oxidative stress (OS) is primarily caused by the formation of free radicals and reactive oxygen species; it is considered as one of the prominent factors in slowing down and degrading cellular machinery of an individual, and it eventually leads to aging and age-related diseases by its continuous higher state. The relation between molecular damage and OS should be particularized to understand the beginning of destruction at the cellular levels, extending outwards to affect tissues, organs, and ultimately to the organism. Several OS biomarkers, which are established at the biomolecular level, are useful in investigating the disease susceptibility during aging. Slowing down the aging process is a matter of reducing the rate of oxidative damage to the cellular machinery over time. The breakdown of homeostasis, the mild overcompensation, the reestablishment of homeostasis, and the adaptive nature of the process are the essential features of hormesis, which incorporates several factors, including calorie restriction, nutrition and lifestyle modifications that play an important role in reducing the OS. In the current review, along with the concept and theories of aging (with emphasis on free radical theory), various manifestations of OS with special attention on mitochondrial dysfunction and age-related diseases have been discussed. To alleviate the OS, hormetic approaches including caloric restriction, exercise, and nutrition have also been discussed.
    Keywords:  Age-related diseases and inflammaging; Aging; Calorie restriction; Hormesis; Oxidative stress and free radicals; Physical activity and nutrition
    DOI:  https://doi.org/10.1016/j.neuint.2023.105490
  2. Recent Prog Nutr. 2022 ;2(4):
    Emerging Nutrition Approaches to Support the Mind and Muscle for Healthy Aging.
    Gabrielle M Mey, Jacob T Mey.
      This narrative review highlights recent advances and ongoing trials using nutrition approaches for healthy aging. Focus will be placed on nutrition therapies that target cognition ("the mind") and mobility ("the muscle"), both critical components to maintaining a high quality of life for older adults. For "the mind," two seemingly incongruent therapies are being investigated to improve cognition-the MIND diet (high in carbohydrates and anti-oxidant fruits and vegetables) and the ketogenic diet (low in carbohydrates, high in fats). For "the muscle," a focus on protein and energy intake has dominated the literature, yet a recent clinical trial supports the use of whole-grains as a tool to improve whole-body protein turnover-a primary regulator of lean body mass and muscle. Finally, emerging data and clinical trials on caloric restriction have solidified this strategy as the only nutritional approach to slow intrinsic factors of whole-body aging, which may positively impact both "the mind" and "the muscle."
    Keywords:  MIND; Medical nutrition therapy; calorie restriction; ketogenic; muscle protein synthesis
    DOI:  https://doi.org/10.21926/rpn.2204022
  3. Front Aging. 2022 ;3 1115408
    Editorial: Somatic mutations, genome mosaicism and aging.
    Michael A Lodato, Jan Vijg.
      
    Keywords:  DNA damage; aging; genome mosaicism; oxidative stress; somatic mutation
    DOI:  https://doi.org/10.3389/fragi.2022.1115408
  4. Curr Pharm Des. 2023 Jan 27.
    Can Brain-Derived Neurotrophic Factor (Bdnf) Mimetics Be A Way Out For Neurodegenerative Diseases?
    Orhan Tansel Korkmaz.
      
    Keywords:  BDNF mimetics; Brain-derived neurotrophic factor; Neurodegenerative diseases; Neurotrophins; TrkB; p75NTR
    DOI:  https://doi.org/10.2174/1381612829666230127142414
  5. Curr Mol Med. 2023 Jan 20.
    Autophagy as an Anti-senescent in Aging Neurocytes.
    Basheer Abdullah Marzoog.
      Neuron homeostasis is crucial for the organism, and its maintenance is multifactorial, including autophagy. The turnover of aberrant intracellular components is a fundamental pathogenetic mechanism for cell aging. Autophagy is involved in the acceleration of the neurocyte aging process and the modification of cell longevity. Neurocyte aging is a process of loss of cell identity through cellular and subcellular changes that include molecular loss of epigenetics, transcriptomic, proteomic, and autophagy dysfunction. Autophagy dysfunction is the hallmark of neurocyte aging. Cell aging is the credential feature of neurodegenerative diseases. Pathophysiologically, aged neurocytes are characterized by dysregulated autophagy and subsequently neurocyte metabolic stress, resulting in accelerated neurocyte aging. In particular, chaperone-mediated autophagy perturbation results in upregulated expression of aging and apoptosis genes. Aged neurocytes are also characterized by the down-regulation of autophagy-related genes, such as ATG5-ATG12, LC3-II / LC3-I ratio, Beclin-1, and p62. Slowing aging through autophagy targeting is sufficient to improve prognosis in neurodegenerative diseases. Three primary anti-senescent molecules are involved in the aging process: mTOR, AMPK, and Sirtuins. Autophagy therapeutic effects can be applied to reverse and slow aging. This article discusses current advances in the role of autophagy in neurocyte homeostasis, aging, and potential therapeutic strategies to reduce aging and increase cell longevity.
    Keywords:  Aging; Autophagy; Differentiation; Homeostasis; Longevity; Neurocyte; Reprogramming; Transdifferentiation
    DOI:  https://doi.org/10.2174/1566524023666230120102718
  6. Aging (Albany NY). 2023 Jan 26. 15
    Are menopause, aging and prostate cancer diseases?
    Mikhail V Blagosklonny.
      There is no doubt that prostate cancer is a disease. Then, according to hyperfunction theory, menopause is also a disease. Like all age-related diseases, it is a natural process, but is also purely harmful, aimless and unintended by nature. But exactly because these diseases (menopause, prostate enlargement, obesity, atherosclerosis, hypertension, diabetes, presbyopia and thousands of others) are partially quasi-programmed, they can be delayed by slowing aging. Is aging a disease? Aging is a quasi-programmed disease that is partially treatable by rapamycin. On the other hand, aging is an abstraction, a sum of all quasi-programmed diseases and processes. In analogy, the zoo consists of animals and does not exist without animals, but the zoo is not an animal.
    Keywords:  geroscience; healthspan; hyperfunction theory of aging; lifespan; mTOR
    DOI:  https://doi.org/10.18632/aging.204499
  7. Life Med. 2022 Oct;1(2): 103-119
    Targeting senescent cells for a healthier longevity: the roadmap for an era of global aging.
    Yu Sun, Qingfeng Li, James L Kirkland.
      Aging is a natural but relentless process of physiological decline, leading to physical frailty, reduced ability to respond to physical stresses (resilience) and, ultimately, organismal death. Cellular senescence, a self-defensive mechanism activated in response to intrinsic stimuli and/or exogenous stress, is one of the central hallmarks of aging. Senescent cells cease to proliferate, while remaining metabolically active and secreting numerous extracellular factors, a feature known as the senescence-associated secretory phenotype. Senescence is physiologically important for embryonic development, tissue repair, and wound healing, and prevents carcinogenesis. However, chronic accumulation of persisting senescent cells contributes to a host of pathologies including age-related morbidities. By paracrine and endocrine mechanisms, senescent cells can induce inflammation locally and systemically, thereby causing tissue dysfunction, and organ degeneration. Agents including those targeting damaging components of the senescence-associated secretory phenotype or inducing apoptosis of senescent cells exhibit remarkable benefits in both preclinical models and early clinical trials for geriatric conditions. Here we summarize features of senescent cells and outline strategies holding the potential to be developed as clinical interventions. In the long run, there is an increasing demand for safe, effective, and clinically translatable senotherapeutics to address healthcare needs in current settings of global aging.
    Keywords:  aging; clinical trial; senescence-associated secretory phenotype; senescent cell; senotherapeutics
    DOI:  https://doi.org/10.1093/lifemedi/lnac030
  8. Alzheimers Res Ther. 2023 Jan 27. 15(1): 22
    How does apolipoprotein E genotype influence the relationship between physical activity and Alzheimer's disease risk? A novel integrative model.
    Jaisalmer de Frutos Lucas, Kelsey R Sewell, Alejandra García-Colomo, Shaun Markovic, Kirk I Erickson, Belinda M Brown.
       BACKGROUND: Wide evidence suggests that physical activity (PA) confers protection against Alzheimer's disease (AD). On the other hand, the apolipoprotein E gene (APOE) ε4 allele represents the greatest genetic risk factor for developing AD. Extensive research has been conducted to determine whether frequent PA can mitigate the increased AD risk associated with APOE ε4. However, thus far, these attempts have produced inconclusive results. In this context, one possible explanation could be that the influence of the combined effect of PA and APOE ε4 carriage might be dependent on the specific outcome measure utilised.
    MAIN BODY: In order to bridge these discrepancies, the aim of this theoretical article is to propose a novel model on the interactive effects of PA and APOE ε4 carriage on well-established mechanisms underlying AD. Available literature was searched to investigate how PA and APOE ε4 carriage, independently and in combination, may alter several molecular pathways involved in AD pathogenesis. The reviewed mechanisms include amyloid beta (Aβ) and tau deposition and clearance, neuronal resilience and neurogenesis, lipid function and cerebrovascular alterations, brain immune response and glucose metabolism. Finally, combining all this information, we have built an integrative model, which includes evidence-based and theoretical synergistic interactions across mechanisms. Moreover, we have identified key knowledge gaps in the literature, providing a list of testable hypotheses that future studies need to address.
    CONCLUSIONS: We conclude that PA influences a wide array of molecular targets involved in AD neuropathology. A deeper understanding of where, when and, most importantly, how PA decreases AD risk even in the presence of the APOE ε4 allele will enable the creation of new protocols using exercise along pharmaceuticals in combined therapeutic approaches.
    Keywords:  APOE ε4; Alzheimer’s disease; Amyloid pathology; Cerebrovascular health; Glucose metabolism; Mitochondrial dysfunction; Neuroinflammation; Neurotrophic factors; Physical activity; Tau pathology
    DOI:  https://doi.org/10.1186/s13195-023-01170-4
  9. Vitam Horm. 2023 ;pii: S0083-6729(22)00073-5. [Epub ahead of print]121 293-318
    Mechanisms of action of vitamin D in delaying aging and preventing disease by inhibiting oxidative stress.
    Dengshun Miao, David Goltzman.
      Although several recent studies have shown that vitamin D supplementation beneficially decreases oxidative stress parameters, there is no consensus on this subject in humans. Thus the role of vitamin D supplementation has recently become a controversial topic because large intervention studies in humans have not shown significant benefits. These studies have indicated that supplementation with precursor forms of active vitamin D has no effect on all-cause mortality, cannot reduce the fracture risk of the elderly, cannot reduce the incidence of cancer or cardiovascular disease in the elderly, and cannot significantly reduce the incidence risk of diabetes in the elderly. However, a link between several age-related diseases and enhanced oxidative stress has been found in mice with insufficient or deficient 1,25-dihydroxyvitamin D (1,25(OH)2D), the active form of vitamin D, which indicates that reduced active vitamin D accelerates aging and age-related diseases by increasing oxidative stress. Furthermore, supplementation of exogenous 1,25(OH)2D3, or antioxidants, could dramatically postpone aging, prevent osteoporosis and spontaneous tumor development induced by 1,25(OH)2D insufficiency or deficiency, by inhibiting oxidative stress. Mechanistically, the antioxidative effects of 1,25(OH)2D3 are carried out via the vitamin D receptor (VDR) by activation of the Nrf2 oxidative stress response pathway though transcriptional or posttranscriptional activation of Nrf2 or transcriptional upregulation of Sirt1 and Bmi1 expression. Whether discrepancies between studies in humans and in mice reflect the different forms of vitamin D examined remains to be determined.
    Keywords:  Antioxidative effects; Diseases; Nrf2; Oxidative stress; Sirt1 and Bmi1; Vitamin D deficiency; Vitamin D receptor; Vitamin D supplementation
    DOI:  https://doi.org/10.1016/bs.vh.2022.09.004
  10. Biogerontology. 2023 Jan 28.
    Insights on the role of L-lactate as a signaling molecule in skin aging.
    Salvatore Chirumbolo, Dario Bertossi, Pierre Magistretti.
      L-lactate is a catabolite from the anaerobic metabolism of glucose, which plays a paramount role as a signaling molecule in various steps of the cell survival. Its activity, as a master tuner of many mechanisms underlying the aging process, for example in the skin, is still presumptive, however its crucial position in the complex cross-talk between mitochondria and the process of cell survival, should suggest that L-lactate may be not a simple waste product but a fine regulator of the aging/survival machinery, probably via mito-hormesis. Actually, emerging evidence is highlighting that ROS are crucial in the signaling of skin health, including mechanisms underlying wound repair, renewal and aging. The ROS, including superoxide anion, hydrogen peroxide, and nitric oxide, play both beneficial and detrimental roles depending upon their levels and cellular microenvironment. Physiological ROS levels are essential for cutaneous health and the wound repair process. Aberrant redox signaling activity drives chronic skin disease in elderly. On the contrary, impaired redox modulation, due to enhanced ROS generation and/or reduced levels of antioxidant defense, suppresses wound healing via promoting lymphatic/vascular endothelial cell apoptosis and death. This review tries to elucidate this issue.
    Keywords:  Aging; L-lactate; Mito-hormesis; Redox signaling; Skin
    DOI:  https://doi.org/10.1007/s10522-023-10018-1
  11. Front Bioeng Biotechnol. 2022 ;10 1082403
    Mechanism of action and therapeutic effects of oxidative stress and stem cell-based materials in skin aging: Current evidence and future perspectives.
    Huan Qian, Yihan Shan, Ruicheng Gong, Danfeng Lin, Mengwen Zhang, Chen Wang, Lu Wang.
      Aging is associated with multiple degenerative diseases, including atherosclerosis, osteoporosis, and Alzheimer's disease. As the most intuitive manifestation of aging, skin aging has received the most significant attention. Skin aging results from various intrinsic and extrinsic factors. Aged skin is characterized by wrinkles, laxity, elastosis, telangiectasia, and aberrant pigmentation. The underlying mechanism is complex and may involve cellular senescence, DNA damage, oxidative stress (OS), inflammation, and genetic mutations, among other factors. Among them, OS plays an important role in skin aging, and multiple antioxidants (e.g., vitamin C, glutathione, and melatonin) are considered to promote skin rejuvenation. In addition, stem cells that exhibit self-replication, multi-directional differentiation, and a strong paracrine function can exert anti-aging effects by inhibiting OS. With the further development of stem cell technology, treatments related to OS mitigation and involving stem cell use may have a promising future in anti-skin aging therapy.
    Keywords:  aging; materials; oxidative stress; skin; stem cell
    DOI:  https://doi.org/10.3389/fbioe.2022.1082403
  12. Ageing Res Rev. 2023 Jan 21. pii: S1568-1637(23)00021-1. [Epub ahead of print]85 101862
    Defective proteostasis in Alzheimer's disease.
    Danielle Cozachenco, Felipe C Ribeiro, Sergio T Ferreira.
      The homeostasis of cellular proteins, or proteostasis, is critical for neuronal function and for brain processes, including learning and memory. Increasing evidence indicates that defective proteostasis contributes to the progression of neurodegenerative disorders, including Alzheimer's disease (AD), the most prevalent form of dementia in the elderly. Proteostasis comprises a set of cellular mechanisms that control protein synthesis, folding, post-translational modification and degradation, all of which are deregulated in AD. Importantly, deregulation of proteostasis plays a key role in synapse dysfunction and in memory impairment, the major clinical manifestation of AD. Here, we discuss molecular pathways involved in protein synthesis and degradation that are altered in AD, and possible pharmacological approaches to correct these defects.
    Keywords:  Alzheimer’s disease; Amyloid-β oligomers; Autophagy; Degradation; ER stress; Protein synthesis; Proteostasis; Ubiquitin-proteasome system
    DOI:  https://doi.org/10.1016/j.arr.2023.101862
  13. Gut Microbes. 2023 Jan-Dec;15(1):15(1): 2167172
    Gut-derived β-amyloid: Likely a centerpiece of the gut-brain axis contributing to Alzheimer's pathogenesis.
    Jinghua Jin, Zhi Xu, Lina Zhang, Can Zhang, Xiaoduo Zhao, Yuxuan Mao, Haojian Zhang, Xingguang Liang, Juanli Wu, Ying Yang, Jing Zhang.
      Peripheral β-amyloid (Aβ), including those contained in the gut, may contribute to the formation of Aβ plaques in the brain, and gut microbiota appears to exert an impact on Alzheimer's disease (AD) via the gut-brain axis, although detailed mechanisms are not clearly defined. The current study focused on uncovering the potential interactions among gut-derived Aβ in aging, gut microbiota, and AD pathogenesis. To achieve this goal, the expression levels of Aβ and several key proteins involved in Aβ metabolism were initially assessed in mouse gut, with key results confirmed in human tissue. The results demonstrated that a high level of Aβ was detected throughout the gut in both mice and human, and gut Aβ42 increased with age in wild type and mutant amyloid precursor protein/presenilin 1 (APP/PS1) mice. Next, the gut microbiome of mice was characterized by 16S rRNA sequencing, and we found the gut microbiome altered significantly in aged APP/PS1 mice and fecal microbiota transplantation (FMT) of aged APP/PS1 mice increased gut BACE1 and Aβ42 levels. Intra-intestinal injection of isotope or fluorescence labeled Aβ combined with vagotomy was also performed to investigate the transmission of Aβ from gut to brain. The data showed that, in aged mice, the gut Aβ42 was transported to the brain mainly via blood rather than the vagal nerve. Furthermore, FMT of APP/PS1 mice induced neuroinflammation, a phenotype that mimics early AD pathology. Taken together, this study suggests that the gut is likely a critical source of Aβ in the brain, and gut microbiota can further upregulate gut Aβ production, thereby potentially contributing to AD pathogenesis.
    Keywords:  Alzheimer’s disease; aging; cognition; gut microbiota; gut–brain axis; β-amyloid
    DOI:  https://doi.org/10.1080/19490976.2023.2167172
  14. Sci Rep. 2023 Jan 27. 13(1): 1526
    Investigation of genetic variants and causal biomarkers associated with brain aging.
    Jangho Kim, Junhyeong Lee, Kisung Nam, Seunggeun Lee.
      Delta age is a biomarker of brain aging that captures differences between the chronological age and the predicted biological brain age. Using multimodal data of brain MRI, genomics, and blood-based biomarkers and metabolomics in UK Biobank, this study investigates an explainable and causal basis of high delta age. A visual saliency map of brain regions showed that lower volumes in the fornix and the lower part of the thalamus are key predictors of high delta age. Genome-wide association analysis of the delta age using the SNP array data identified associated variants in gene regions such as KLF3-AS1 and STX1. GWAS was also performed on the volumes in the fornix and the lower part of the thalamus, showing a high genetic correlation with delta age, indicating that they share a genetic basis. Mendelian randomization (MR) for all metabolomic biomarkers and blood-related phenotypes showed that immune-related phenotypes have a causal impact on increasing delta age. Our analysis revealed regions in the brain that are susceptible to the aging process and provided evidence of the causal and genetic connections between immune responses and brain aging.
    DOI:  https://doi.org/10.1038/s41598-023-27903-x
  15. Front Psychiatry. 2022 ;13 1102347
    Are Alzheimer's and coronary artery diseases genetically related to longevity?
    Eftychia Bellou, Valentina Escott-Price.
       Introduction: In the last decade researchers have attempted to investigate the shared genetic architecture of longevity and age-related diseases and assess whether the increased longevity in certain people is due to protective alleles in the risk genes for a particular condition or whether there are specific "longevity" genes increasing the lifespan independently of age-related conditions' risk genes. The aim of this study was to investigate the shared genetic component between longevity and two age-related conditions.
    Methods: We performed a cross-trait meta-analysis of publicly available genome-wide data for Alzheimer's disease, coronary artery disease and longevity using a subset-based approach provided by the R package ASSET.
    Results: Despite the lack of strong genetic correlation between longevity and the two diseases, we identified 38 genome-wide significant lead SNPs across 22 independent genomic loci. Of them 6 were found to be potentially shared among the three traits mapping to genes including DAB2IP, DNM2, FCHO1, CLPTM1, and SNRPD2. We also identified 19 novel genome-wide associations for the individual traits in this study. Functional annotations and biological pathway enrichment analyses suggested that pleiotropic variants are involved in clathrin-mediated endocytosis and plasma lipoprotein and neurotransmitter clearance processes.
    Discussion: In summary, we have been able to advance in the knowledge of the genetic overlap existing among longevity and the two most common age-related disorders.
    Keywords:  Alzheimer's disease; coronary artery disease; longevity; pleiotropy; subset-based analysis (ASSET)
    DOI:  https://doi.org/10.3389/fpsyt.2022.1102347
  16. Behav Brain Res. 2023 Jan 24. pii: S0166-4328(23)00027-X. [Epub ahead of print] 114309
    Unveiling new secrets in Parkinson's disease: the glycatome.
    Ana Chegão, Hugo Vicente Miranda.
      We are witnessing a considerable increase in the incidence of Parkinson's disease (PD), which may be due to the general ageing of the population. While there is a plethora of therapeutic strategies for this disease, they still fail to arrest disease progression as they do not target and prevent the neurodegenerative process. The identification of disease-causing mutations allowed researchers to better dissect the underlying causes of this disease, highlighting, for example, the pathogenic role of alpha-synuclein. However, most PD cases are sporadic, which is making it hard to unveil the major causative mechanisms of this disease. In the recent years, epidemiological evidence suggest that type-2 diabetes (T2D) individuals have higher risk and worst outcomes of PD, allowing to raise the hypothesis that some dysregulated processes in T2D may contribute or even trigger the neurodegenerative process in PD. One major consequence of T2D is the unprogrammed reaction between sugars, increased in T2D, and proteins, a reaction named glycation. Pre-clinical reports show that alpha-synuclein is a target of glycation, and glycation potentiates its pathogenicity which contributes for the neurodegenerative process. Moreover, it triggers, anticipates, or aggravates several PD-like motor and non-motor complications. A given profile of proteins are differently glycated in diseased conditions, altering the brain proteome and leading to brain dysfunction and neurodegeneration. Herein we coin the term Glycatome as the profile of glycated proteins. In this review we report on the mechanisms underlying the association between T2D and PD, with particular focus on the impact of protein glycation.
    Keywords:  Glycation; Glycatome; Parkinson’s disease; alpha-synuclein; type-2 diabetes
    DOI:  https://doi.org/10.1016/j.bbr.2023.114309
  17. iScience. 2023 Feb 17. 26(2): 105936
    Mulberroside A alleviates osteoarthritis via restoring impaired autophagy and suppressing MAPK/NF-κB/PI3K-AKT-mTOR signaling pathways.
    Rui Lu, Zhenni Wei, Zhenggang Wang, Shimeng Xu, Kai Sun, Peng Cheng, Xiaojian Huang, Hongbo You, Fengjing Guo, Shuang Liang, An-Min Chen.
      Osteoarthritis (OA) is a trauma-/age-related degenerative disease characterized by chronic inflammation as one of its pathogenic mechanisms. Mulberroside A (MA), a natural bioactive withanolide, demonstrates anti-inflammatory properties in various diseases; however, little is known about the effect of MA on OA. We aim to examine the role of MA on OA and to identify the potential mechanisms through which it protects articular cartilage. In vitro, MA improved inflammatory response, anabolism, and catabolism in IL-1β-induced OA chondrocytes. The chondroprotective effects of MA were attributed to suppressing the MAPK, NF-κB, and PI3K-AKT-mTOR signaling pathways, as well as promoting the autophagy process. In vivo, intra-articular injection of MA reduced the cartilage destruction and reversed the change of anabolic and catabolic-related proteins in destabilized medial meniscus (DMM)-induced OA models. Thus, the study indicates that MA exhibits a chondroprotective effect and might be a promising agent for OA treatment.
    Keywords:  Biomolecules; Disease; Immune response
    DOI:  https://doi.org/10.1016/j.isci.2023.105936
  18. Brain Behav Immun Health. 2023 Mar;28 100577
    The association between sleep quality and telomere length: A systematic literature review.
    Debbie Sabot, Rhianna Lovegrove, Peta Stapleton.
      Several sleep parameters present an elevated risk for processes that contribute to cellular aging. Short sleep duration, sleep apnoea, and insomnia are significantly associated with shorter telomeres, a biological marker of cellular aging. However, there has been no review or analysis of studies that have examined the association between the psychological construct of sleep quality and telomere length. The present study aimed to provide a systematic review of the association between sleep quality and telomere length. A systematic review of English articles was conducted using MEDLINE/PubMed, PsycINFO, Google Scholar, and Web of Science electronic databases, with the final search conducted on 3rd September 2021. Search terms included sleep quality, poor sleep, insomnia, sleep difficulties, sleep issue*, non-restorative sleep, telomere*, cellular aging, and immune cell telomere length. Study eligibility criteria included human participants aged 18 years or older and a reproducible methodology. Study appraisal and synthesis were completed using a systematic search in line with a PICOS approach (P = Patient, problem, or population; I = Intervention, prognostic factor, exposure; C = Comparison, control, or comparator; O = Outcomes; S = Study designs). Twenty-two studies met review inclusion criteria. Qualitative synthesis of the literature indicated insufficient evidence overall to support a significant association between sleep quality and telomere length. Limitations across studies were addressed, such as the assessment of examined constructs. Findings highlight important targets for future research, including the standardised operationalisation of the sleep quality construct and experimental study designs. Research in this area has clinical significance by identifying possible mechanisms that increase the risk for age-related disease and mortality. PROSPERO Registration No.: CRD 42021233139.
    Keywords:  Cellular aging; Non-restorative sleep; Sleep quality; Telomere length
    DOI:  https://doi.org/10.1016/j.bbih.2022.100577
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