bims-caglex Biomed News
on Cellular aging and life extension
Issue of 2024–11–10
fifteen papers selected by
Mario Alexander Guerra Patiño, Universidad Antonio Nariño
  1. The role of high mobility group proteins in cellular senescence mechanisms.
  2. Exploring the effect of different diet types on ageing and age-related diseases.
  3. Opportunities and challenges of foodborne polyphenols applied to anti-aging health foods.
  4. Plasma protein-based organ-specific aging and mortality models unveil diseases as accelerated aging of organismal systems.
  5. Skin senescence-from basic research to clinical practice.
  6. Potential probiotic Lactiplantibacillus plantarum DS1800 extends lifespan and enhances stress resistance in Caenorhabditis elegans model.
  7. Garcinia flavonoids for healthy aging: Anti-senescence mechanisms and cosmeceutical applications in skin care.
  8. Activation of the apelin/APJ system by vitamin D attenuates age-related muscle atrophy.
  9. Zanthoxylum alkylamides alleviate cell cycle arrest and oxidative stress to retard d-galactose-induced aging.
  10. ELO-6 expression predicts longevity in isogenic populations of Caenorhabditis elegans.
  11. HES1 revitalizes the functionality of aged adipose-derived stem cells by inhibiting the transcription of STAT1.
  12. Reduced expressions of TCA cycle genes during aging in humans and mice.
  13. Advancements in Targeting Macrophage Senescence for Age-Associated Conditions.
  14. Exercise-induced adaptive response of different immune organs during ageing.
  15. Fermented antler extract attenuates muscle atrophy by regulating the PI3K/Akt pathway and inflammatory response in immobilization-treated C57BL/6J mice.
  1. Front Aging. 2024 ;5 1486281
    The role of high mobility group proteins in cellular senescence mechanisms.
    Jia Chen, Hongyu Li, Yongyin Huang, Qiang Tang.
      Aging is a universal physiological phenomenon, and chronic age-related diseases have become one of the leading causes of human mortality, accounting for nearly half of all deaths. Studies have shown that reducing the incidence of these diseases can not only extend lifespan but also promote healthy aging. In recent years, the potential role of non-histone high-mobility group proteins (HMGs) in the regulation of aging and lifespan has attracted widespread attention. HMGs play critical roles in cellular senescence and associated diseases through various pathways, encompassing multi-layered mechanisms involving protein interactions, molecular regulation, and chromatin dynamics. This review provides a comprehensive analysis of the interactions between HMG family proteins and senescence-associated secretory phenotype (SASP), chromatin structure, and histone modifications, offering a deeper exploration of the pivotal functions and impacts of HMGs in the aging process. Furthermore, we summarize recent findings on the contributions of HMG proteins to aging and age-related diseases. HMG proteins not only regulate senescence-associated inflammation through modulating the SASP but also influence genomic stability and cell fate decisions via interactions with chromatin and histones. Targeting HMG proteins holds great potential in delaying the progression of aging and its associated diseases. This review aims to provide a systematic overview of HMG proteins' roles in aging and to lay a solid foundation for future anti-aging drug development and therapeutic strategies. With the advancing understanding of the mechanisms by which HMGs regulate aging, developing therapeutic interventions targeting HMGs may emerge as a promising approach to extending lifespan and enhancing healthspan.
    Keywords:  SASP; aging; histone; hmgs; senescence
    DOI:  https://doi.org/10.3389/fragi.2024.1486281
  2. Nutrition. 2024 Oct 10. pii: S0899-9007(24)00245-4. [Epub ahead of print]129 112596
    Exploring the effect of different diet types on ageing and age-related diseases.
    Emmanuel O Mensah, Emmanuel K Danyo, Richard V Asase.
      In recent times, there has been growing interest in understanding the factors contributing to prolonged and healthy lifespans observed in specific populations, tribes, or countries. Factors such as environmental and dietary play significant roles in shaping the ageing process and are often the focus of inquiries seeking to unravel the secrets behind longevity. Among these factors, diet emerges as a primary determinant, capable of either promoting or mitigating the onset of age-related diseases that impact the ageing trajectory. This review examines the impact of various diet types on ageing and age-related conditions, including cardiovascular disease, cancer, neurodegenerative disorders, and metabolic syndrome. Different dietary patterns, such as the Mediterranean diet, the Japanese diet, vegetarian and vegan diets, as well as low-carbohydrate and ketogenic diets, are evaluated for their potential effects on longevity and health span. Each diet type is characterized by distinct nutritional profiles, emphasizing specific food groups, macronutrient compositions, and bioactive components, which may exert diverse effects on ageing processes and disease risk. Additionally, dietary factors such as calorie restriction, intermittent fasting, and dietary supplementation are explored for their potential anti-ageing and disease-modifying effects. Understanding the influence of various diet types on ageing and age-related diseases can inform personalized dietary recommendations and lifestyle interventions aimed at promoting healthy aging and mitigating age-associated morbidities.
    Keywords:  Age-related diseases; Ageing; Diet; Lifespan; Molecular pathways
    DOI:  https://doi.org/10.1016/j.nut.2024.112596
  3. Food Sci Biotechnol. 2024 Dec;33(15): 3445-3461
    Opportunities and challenges of foodborne polyphenols applied to anti-aging health foods.
    Hong Zhuang, Xiaoliang Zhang, Sijia Wu, Pang Yong, Haiyang Yan.
       Abstract: With the increasing proportion of the global aging population, aging mechanisms and anti-aging strategies become hot topics. Nonetheless, the safety of non-natural anti-aging active molecule and the changes in physiological function that occur during aging have not been clarified. There is therefore a need to develop safer pharmaceutical interventions for anti-aging. Numerous types of research have shown that food-derived biomolecules are of great interest due to their unique contribution to anti-aging safety issues and the prevention of degenerative diseases. Among these, polyphenolic organic compounds are widely used in anti-aging research for their ability to mitigate the physiological functional changes that occur during aging. The mechanisms include the free radical theory, immune aging theory, cellular autophagy theory, epigenetic modification theory, gut microbial effects on aging theory, telomere shortening theory, etc. This review elucidates the mechanisms underlying the anti-aging effects of polyphenols found in food-derived bioactive molecules, while also addressing the challenges associated with anti-aging pharmaceuticals. The review concludes by offering insights into the current landscape of anti-aging active molecule research, aiming to serve as a valuable resource for further scholarly inquiry.
    Graphical abstract:
    Keywords:  Anti-aging; Food-derived bioactive molecules; Polyphenols
    DOI:  https://doi.org/10.1007/s10068-024-01686-x
  4. Cell Metab. 2024 Oct 29. pii: S1550-4131(24)00401-7. [Epub ahead of print]
    Plasma protein-based organ-specific aging and mortality models unveil diseases as accelerated aging of organismal systems.
    Ludger J E Goeminne, Anastasiya Vladimirova, Alec Eames, Alexander Tyshkovskiy, M Austin Argentieri, Kejun Ying, Mahdi Moqri, Vadim N Gladyshev.
      Aging is a complex process manifesting at molecular, cellular, organ, and organismal levels. It leads to functional decline, disease, and ultimately death, but the relationship between these fundamental biomedical features remains elusive. By applying elastic net regularization to plasma proteome data of over 50,000 human subjects in the UK Biobank and other cohorts, we report interpretable organ-specific and conventional aging models trained on chronological age, mortality, and longitudinal proteome data. These models predict organ/system-specific disease and indicate that men age faster than women in most organs. Accelerated organ aging leads to diseases in these organs, and specific diets, lifestyles, professions, and medications influence organ aging rates. We then identify proteins driving these associations with organ-specific aging. Our analyses reveal that age-related chronic diseases epitomize accelerated organ- and system-specific aging, modifiable through environmental factors, advocating for both universal whole-organism and personalized organ/system-specific anti-aging interventions.
    Keywords:  aging models; blood plasma; diet; disease; elastic net; lifestyle; longevity interventions; mortality; organ-specific aging; proteomic clocks
    DOI:  https://doi.org/10.1016/j.cmet.2024.10.005
  5. Front Med (Lausanne). 2024 ;11 1484345
    Skin senescence-from basic research to clinical practice.
    Natalia Dorf, Mateusz Maciejczyk.
      The most recognizable implications of tissue aging manifest themselves on the skin. Skin laxity, roughness, pigmentation disorders, age spots, wrinkles, telangiectasia or hair graying are symptoms of physiological aging. Development of the senescent phenotype depends on the interaction between aging cells and remodeling of the skin's extracellular matrix (ECM) that contains collagen and elastic fiber. Aging changes occur due to the combination of both endogenous (gene mutation, cellular metabolism or hormonal agents) and exogenous factors (ultraviolet light, environmental pollutants, and unsuitable diet). However, overproduction of mitochondrial reactive oxygen species (ROS) is a key factor driving cellular senescence. Aging theories have disclosed a range of diverse molecular mechanisms that are associated with cellular senescence of the body. Theories best supported by evidence include protein glycation, oxidative stress, telomere shortening, cell cycle arrest, and a limited number of cell divisions. Accumulation of the ECM damage is suggested to be a key factor in skin aging. Every cell indicates a functional and morphological change that may be used as a biomarker of senescence. Senescence-associated β-galactosidase (SA-β-gal), cell cycle inhibitors (p16INK4a, p21CIP1, p27, p53), DNA segments with chromatin alterations reinforcing senescence (DNA-SCARS), senescence-associated heterochromatin foci (SAHF), shortening of telomeres or downregulation of lamina B1 constitute just an example of aging biomarkers known so far. Aging may also be assessed non-invasively through measuring the skin fluorescence of advanced glycation end-products (AGEs). This review summarizes the recent knowledge on the pathogenesis and clinical conditions of skin aging as well as biomarkers of skin senescence.
    Keywords:  aging; biomarkers; senescence; skin; skin aging
    DOI:  https://doi.org/10.3389/fmed.2024.1484345
  6. Front Physiol. 2024 ;15 1476096
    Potential probiotic Lactiplantibacillus plantarum DS1800 extends lifespan and enhances stress resistance in Caenorhabditis elegans model.
    Seunghyun Kim, Yu-Ri Lee, Haneol Yang, Chan-Hyeok Park, Chan-Seok Yun, Byung-Chun Jang, Yeongjin Hong, Doo-Sang Park.
      Probiotics are live microorganisms that provide health benefits when administered in appropriate amounts by improving or restoring the balance of intestinal microbiota. Various functional probiotic products have been developed due to the growing interest in the health-promoting and anti-aging effects of enhancing the gut microbiome. Lactiplantibacillus plantarum species are known for their potential to extend lifespan. However, this activity is strain or isolation source specific, necessitating the identification of individual strain functionalities. This study used the C. elegans model to screen probiotics for life-extension effects and analyze their functions. The 43 lactic-acid bacteria strains isolated from fermented foods, breast milk, and human feces were subjected to longevity assays, and L. plantarum DS1800 was selected to demonstrate the most effective lifespan extension. The average lifespan of Caenorhabditis elegans fed DS1800 increased by 17.36% compared with those fed Escherichia coli OP50. Further analysis of the expression of key genes related to longevity revealed the high expression of the skinhead-1 (skn-1), antibacterial, and heat stress resistance genes via the p38 MAPK pathway. These expression patterns suggest that DS1800 extends the lifespan of C. elegans by enhancing its stress resistance and protecting it against pathogens. Additionally, DS1800 exhibited excellent intestinal adhesion, with 7.56% adhesion to HT-29 cells. Therefore, L. plantarum DS1800 is effective in extending the lifespan of C. elegans and can be used as a functional probiotic.
    Keywords:  C. elegans; L. plantarum; life extension; probiotics; stress resistance
    DOI:  https://doi.org/10.3389/fphys.2024.1476096
  7. Fitoterapia. 2024 Nov 01. pii: S0367-326X(24)00465-9. [Epub ahead of print] 106282
    Garcinia flavonoids for healthy aging: Anti-senescence mechanisms and cosmeceutical applications in skin care.
    Idris Adewale Ahmed, Nor Hisam Zamakshshari, Maryam Abimbola Mikail, Ibrahim Bello, Md Sanower Hossain.
      Cellular senescence, the irreversible arrest of cell division, is a hallmark of aging and a key contributor to age-related disorders. Targeting senescent cells represents a promising therapeutic approach to combat these ailments. This review explores the potential of Garcinia species, a genus rich in flavonoids with established antioxidant and anti-inflammatory properties, as a source of natural anti-senescence agents. We investigate the intricate connections between aging, cellular senescence, and oxidative stress, highlighting the detrimental effects of free radicals on cellular health. Furthermore, we analyze the diverse array of flavonoids identified within Garcinia and their established cellular mechanisms. We critically evaluate the emerging evidence for the anti-senescence potential of flavonoids in general and the limited research on Garcinia flavonoids in this context. By identifying existing knowledge gaps and paving the way for future research, this review underscores the exciting potential of Garcinia flavonoids as natural anti-senescence agents. These agents hold promise for not only promoting healthy aging but also for the development of cosmeceutical products that combat the visible signs of aging.
    Keywords:  Aging; Antioxidants; Cosmeceuticals; Flavonoids; Garcinia spp.; Senescence
    DOI:  https://doi.org/10.1016/j.fitote.2024.106282
  8. Life Sci. 2024 Oct 31. pii: S0024-3205(24)00795-1. [Epub ahead of print]359 123205
    Activation of the apelin/APJ system by vitamin D attenuates age-related muscle atrophy.
    Yoo Jeong Lee, Gyu Hee Kim, Da Som Lee, Hyeon-Ju Jeong, Joo Hyun Lim.
       AIMS: Age-related frailty and reduced physical activity contribute to a degenerative loss of muscle mass, function, and strength, which is known as sarcopenia. Increasing evidence has shown that vitamin D has beneficial effects on the muscle health. However, the molecular mechanisms of vitamin D have not been fully elucidated. In this study, we aimed to demonstrate whether vitamin D can overcome muscle atrophy due to aging, especially with respect to the regulation of myokines.
    MAIN METHODS: Young (3-month-old) and aged (18-month-old) C57BL/6 mice were assigned to the following 3 groups: normal diet (1000 IU/kg), vitamin D3-supplemented diet (20,000 IU/kg), and normal diet plus exercise for 4 months.
    KEY FINDINGS: We found that the reduction in muscle strength and mass due to aging was reversed by vitamin D3 supplementation. The levels of markers involved in muscle atrophy and cellular senescence in the muscle of the aged mice were substantially decreased by vitamin D3. Interestingly, we observed that the expression of apelin and its receptor (APJ), which is known to be secreted after exercise, significantly increased in aged muscles with a vitamin D3-supplemented diet but not in the young mice. Moreover, circulating interleukin-6 (IL-6) and growth differentiation factor 8 (GDF8) levels were significantly increased in the aged mice but were restored by vitamin D3 treatment.
    SIGNIFICANCE: Our present data indicate that vitamin D3 supplementation ameliorates aging-induced muscle atrophy and senescence, similar to the effects of exercise, suggesting the positive impact of vitamin D as an intervention strategy to prevent aging-induced metabolic diseases.
    Keywords:  APJ; Apelin; Myokine; Sarcopenia; Vitamin D
    DOI:  https://doi.org/10.1016/j.lfs.2024.123205
  9. Food Sci Biotechnol. 2024 Dec;33(15): 3541-3552
    Zanthoxylum alkylamides alleviate cell cycle arrest and oxidative stress to retard d-galactose-induced aging.
    Yuping Zhu, Pan Yang, Suzhen Zhai, Chunlin Zhang.
      During the aging process, the abilities to maintain homeostasis and resist stress decrease, leading to degenerative changes in tissues and organs. The pathological process of aging is characterized by oxidative stress and cell cycle arrest. Zanthoxylum alkylamides (ZA) can mitigate hepatic oxidative stress. However, whether ZA can delay aging and the underlying mechanisms are unclear. Herein, ZA were shown to inhibit d-galactose-induced aging in a dose-dependent manner. ZA activated CyclinD1 and CyclinE2 to exert anti-cell cycle arrest effects and activated the Nrf2/HO1 pathway to reduce the accumulated intracellular reactive oxygen species (ROS) and improve antioxidant capacity. Moreover, motor coordination and spontaneous exploration were improved in aging mice administered ZA. Overall, ZA alleviated cell cycle arrest and oxidative stress to delay d-galactose-induced aging.
    Supplementary Information: The online version contains supplementary material available at 10.1007/s10068-024-01599-9.
    Keywords:  Aging; Cell cycle; Oxidative stress; Zanthoxylum alkylamides
    DOI:  https://doi.org/10.1007/s10068-024-01599-9
  10. Nat Commun. 2024 Nov 02. 15(1): 9470
    ELO-6 expression predicts longevity in isogenic populations of Caenorhabditis elegans.
    Weilin Kong, Guoli Gu, Tong Dai, Beibei Chen, Yanli Wang, Zheng Zeng, Mintie Pu.
      Variations of individual lifespans within genetically identical populations in homogenous environments are remarkable, with the cause largely unknown. Here, we show the expression dynamic of the Caenorhabditis elegans fatty acid elongase ELO-6 during aging predicts individual longevity in isogenic populations. elo-6 expression is reduced with age. ELO-6 expression level exhibits obvious variation between individuals in mid-aged worms and is positively correlated with lifespan and health span. Interventions that prolong longevity enhance ELO-6 expression stability during aging, indicating ELO-6 is also a populational lifespan predictor. Differentially expressed genes between short-lived and long-lived isogenic worms regulate lifespan and are enriched for PQM-1 binding sites. pqm-1 in young to mid-aged adults causes individual ELO-6 expression heterogeneity and restricts health span and life span. Thus, our study identifies ELO-6 as a predictor of individual and populational lifespan and reveals the role of pqm-1 in causing individual health span variation in the mid-aged C. elegans.
    DOI:  https://doi.org/10.1038/s41467-024-53887-x
  11. Stem Cell Res Ther. 2024 Nov 05. 15(1): 399
    HES1 revitalizes the functionality of aged adipose-derived stem cells by inhibiting the transcription of STAT1.
    Chengcheng Li, Sen Ren, Chengqi Yan, Cheng Wang, Tao Jiang, Yu Kang, Jing Chen, Hewei Xiong, Jiahe Guo, Guoyong Jiang, Shuoyuan Liu, Pengjuan Nie, Zhenbing Chen.
       BACKGROUND: The effectiveness of adipose-derived stem cells (ADSCs) in therapy diminishes with age. It has been reported that transcription factors (TFs) play a crucial role in the aging and functionality of stem cells. Nevertheless, there is limited understanding regarding the involvement of TFs in the aging mechanism of ADSCs.
    METHODS: RNA sequencing (RNA-seq) was utilized to discern the differentially expressed genes in ADSCs obtained from donors of varying ages. TFs exhibiting significant variations across age groups were identified and subsequently validated. ADSCs were manipulated to exhibit either enhanced expression or reduced levels of HES1 and STAT1 via lentivirus transfection and small interfering RNA (siRNA) techniques. The impact of these genetic alterations on ADSCs' proliferation, migration, and cellular senescence was assessed using EdU, transwell, and senescence-activated β-galactosidase (SA-β-gal) staining assays. The DNA sequences bound by HES1 were investigated through the CUT & Tag assay. Lastly, the therapeutic efficacy of aged ADSCs with HES1 overexpression was evaluated in skin injury model of male Sprague-Dawley rats.
    RESULTS: 678 genes showed differential expression between ADSCs obtained from young and old donors (Y-ADSCs and O-ADSCs), with 47 of these genes being TFs. Notably, the expression of the TF hairy and enhancer of split 1 (HES1) was notably reduced in ADSCs from old donors. Introducing HES1 overexpression in aged ADSCs resulted in improved cellular function and the suppression of cellular senescence, while reducing HES1 levels in young ADSCs had the opposite effect. Mechanistically, HES1 was found to interact with the promoter region of another TF, signal transducer and activator of transcription 1 (STAT1), to inhibit its transcription. Knocking down STAT1 could fully reverse the negative effects caused by decreased HES1 in ADSCs, leading to a reduction in the secretion of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-8. Ultimately, restoring HES1 expression in aged ADSCs demonstrated enhanced therapeutic potential in promoting skin wound healing.
    CONCLUSION: HES1 acts as an inhibitor of cellular senescence in the aging progression of ADSCs through the modulation of STAT1 expression, suggesting a promising avenue for rejuvenating senescent ADSCs and improving wound healing.
    Keywords:  Adipose stem cell; Aging; HES1; STAT1; Transcription factors
    DOI:  https://doi.org/10.1186/s13287-024-04002-w
  12. Biochem Biophys Res Commun. 2024 Oct 29. pii: S0006-291X(24)01453-0. [Epub ahead of print]738 150917
    Reduced expressions of TCA cycle genes during aging in humans and mice.
    Chao Zhang, Zhiyao Fu, Ren Zhang.
      Aging is associated with a decline in physiological functions and an increased risk of metabolic disorders. The liver, a key organ in metabolism, undergoes significant changes during aging that can contribute to systemic metabolic dysfunction. This study investigates the expression of genes involved in the tricarboxylic acid (TCA) cycle, a critical pathway for energy production, in the aging liver. We analyzed RNA sequencing data from the Genotype-Tissue Expression (GTEx) project to assess age-related changes in gene expression in the human liver. To validate our findings, we conducted complementary studies in young and old mice, examining the expression of key TCA cycle genes using quantitative real-time PCR. Our analysis of the GTEx dataset revealed a significant reduction in the expression of many genes that are critical for metabolism, including fat mass and obesity associated (FTO) and adiponectin receptor 1 (ADIPOR1). The most overrepresented pathway among the statistically enriched ones was the TCA cycle, with multiple genes exhibiting downregulation in older humans. This reduction was consistent with findings in aging mice, which also showed decreased expression of several TCA cycle genes. These results suggest a conserved pattern of age-related downregulation of TCA cycle, potentially leading to diminished mitochondrial function and energy production in the liver. The reduced expression of TCA cycle genes in the aging liver may contribute to metabolic dysfunction and increased susceptibility to age-related diseases. Understanding the molecular basis of these changes provides new insights into the aging process and highlights potential targets for interventions aimed at promoting healthy aging and preventing metabolic disorders.
    DOI:  https://doi.org/10.1016/j.bbrc.2024.150917
  13. Aging Dis. 2024 Nov 04.
    Advancements in Targeting Macrophage Senescence for Age-Associated Conditions.
    Jingwei Xiao, Hung Sing Li, Senthil Kumaran Satyanarayanan, Shu Lai Leung, Qiuju Yuan, Yaofeng Wang, Dajiang Qin, Suki Man Yan Lee.
      Macrophages, a critical subset of innate immune cells, play a pivotal role in cytokine production during disease progression, tissue injury, and pathogen invasion. Their intricate involvement in the manifestation of chronic low-grade inflammation associated with the aging process is widely acknowledged. Notably, in aged tissues, macrophages exhibit an altered phenotype characterized by an augmented synthesis of pro-inflammatory cytokines and chemokines, a profile intimately associated with a phenomenon known as inflammaging. Macrophages possess the capacity to undergo cellular senescence, a state of permanent growth arrest, in response to diverse stressors, including aging. Senescent macrophages secrete an array of pro-inflammatory molecules, growth factors, and matrix metalloproteinases, collectively referred to as the Senescence-Associated Secretory Phenotype (SASP). The SASP exacerbates the state of chronic inflammation observed in aging tissues. Thus, disruptions in macrophage function and signaling pathways due to aging result in escalated production of inflammatory mediators, perpetuating inflammaging. Recent research has uncovered novel mechanisms centred around innate immune signaling and mitochondrial dysfunction in macrophages, highlighting their crucial role in the development of inflammaging and associated pathological conditions. This review delves into the latest scientific findings on these emerging mechanisms in macrophage senescence related to aging and explores the prospects of targeting macrophages to address age- associated conditions effectively.
    DOI:  https://doi.org/10.14336/AD.2024.0720
  14. Ageing Res Rev. 2024 Oct 30. pii: S1568-1637(24)00391-X. [Epub ahead of print] 102573
    Exercise-induced adaptive response of different immune organs during ageing.
    Huanghao Zhou, Xiao Han, Chunxiu Huang, Huijuan Wu, Yue Hu, Cong Chen, Jing Tao.
      The immune system plays a crucial role in the ageing process. As individuals age, significant alterations in the immune system experiences occur, marked by a decline in immune cell count, compromised immune function, and decreased immune regulation across various immune organs. These changes collectively weaken the capacity to combat diseases and infections, highlighting the vulnerability that accompanies ageing. Exercise is a potent intervention that profoundly influences holistic well-being and disease mitigation, with a notable emphasis on immune modulation. In general, regular moderate exercise holds significant potential to enhance immune defense mechanisms and metabolic well-being by augmenting the circulation and activation of immune cells. However, some exercise modalities would trigger detrimental effects on the immune system. It can be seen that the regulatory responses of various immune organs to diverse exercise patterns are different. This review aims to examine the immunological responses elicited by exercise across various immune organs, including the lymph nodes, spleen, bone marrow, and thymus, to underscore the nuanced interplay between exercise patterns and the immune organ. This underscores the importance of customizing exercise interventions to optimize immune function across the lifespan.
    Keywords:  ageing; exercise; immune organs; immune response
    DOI:  https://doi.org/10.1016/j.arr.2024.102573
  15. Food Sci Biotechnol. 2024 Dec;33(15): 3617-3628
    Fermented antler extract attenuates muscle atrophy by regulating the PI3K/Akt pathway and inflammatory response in immobilization-treated C57BL/6J mice.
    Jihee Yoo, Changhee Kim, Hyerin Lee, Bong Soo Ko, Dong-Woo Lee, Jae-Kwan Hwang.
      Muscle atrophy or muscle wasting, which is featured by reduced muscle function and mass, typically results from disuse, aging, and chronic diseases. The deer antler, which refers to the young and non-ossified antlers of various species of deer-related animals, is not fully calcified and comprises of densely growing hair. Here, we investigated whether Bacillus subtilis-fermented antler extract (FAE) inhibits immobilization-induced muscle atrophy in C57BL/6J mice. Oral administration of FAE increased grip strength, exercise performance, muscle mass, and volume in mice. FAE stimulated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, enhancing the mammalian target of rapamycin pathway for muscle synthesis. FAE phosphorylated Forkhead box O3 and downregulated muscle RING finger-1 and atrogin-1 for proteolysis. FAE inhibited the mRNA expression of tumor necrosis factor alpha and interleukin-6 through nuclear factor kappa B. Consequently, FAE attenuated muscle atrophy by regulating the PI3K/Akt pathway and inflammation.
    Keywords:  Antler; Fermentation; Immobilization; Muscle atrophy
    DOI:  https://doi.org/10.1007/s10068-024-01606-z
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