Biogerontology最新文献

{"title":"Comparison of MSCs and Muse cells: the possible use for healthspan optimization.","authors":"Mari Dezawa","doi":"10.1007/s10522-025-10275-2","DOIUrl":"10.1007/s10522-025-10275-2","url":null,"abstract":"<p><p>The exploration for safe, effective intervention strategies to improve longevity and aging-related diseases is attracting attention to prolong the healthy lifespan. Since aging is based on cellular changes, including telomere attrition, DNA damage, and mitochondrial dysfunction, therapies related to stem cells are expected to be a rational strategy for solving aging problems at the cellular level. Mesenchymal stem cells (MSCs) are an easily accessible, safe candidate, as they supply paracrine factors and extracellular vesicles to deliver pleiotropic effects for aging tissues. Multilineage-differentiating stress enduring (Muse) cells represent endogenous, reparative macrophage-like/pluripotent-like stem cells distributed in various tissues, including extraembryonic tissues such as the umbilical cord, and are also found in MSCs as a small percentage of the total population. Muse cell characteristics are different from those of MSCs. Intravenously injected Muse cells sharply sense the universal damage signal sphingosine-1-P and selectively migrate to damaged tissue rather than being trapped in the lung, phagocytose damaged/apoptotic cells in the tissue and directly differentiate into the same cell type. Muse cells then repair the three dimensional structure of the tissue by replacing multiple tissue component with healthy cells through pluripotent-like differentiation. Clinical trials have shown that HLA-mismatched donor Muse cells escape immune rejection and survive in the recipient tissue for an extended period without immunosuppressant treatment. Therefore, the pleiotropic bystander effects of Muse cells are more potent than those of MSCs. Due to heterogeneity, the properties of MSCs are still not fully understood; they have limited differentiation ability into osteogenic, chondrogenic, and adipogenic cells, and the main biological action in vivo is bystander effects. Muse cells are key, not only to the medical benefits of MSCs, but also to their potential use in anti-aging therapy. Enriching and purifying Muse cells will significantly enhance the therapeutic effect of MSCs, leading to further expansion of the use of MSCs. This review discusses the fundamental differences between MSCs and Muse cells and their potential applications in anti-aging therapy.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"139"},"PeriodicalIF":4.4,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12222320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144538013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The combination of hawthorn extract administration and high-intensity interval training (HIIT) alleviates hippocampus damage in aged rats: the behavioral, molecular and histological evaluations.","authors":"Mohammad Rami, Samaneh Rahdar, Hamid Aghili Nasab, Seyedeh Fatemeh Hoseininezhad, Seyedeh Narges Sadat Ahmadi, Mohammad Amin Rajizadeh","doi":"10.1007/s10522-025-10264-5","DOIUrl":"10.1007/s10522-025-10264-5","url":null,"abstract":"<p><p>The aging process results in a gradual decline in brain function, characterized by heightened hippocampal atrophy and dysfunction. Physical activity can enhance cognitive skills in elderly individuals and is significant in the prevention of neurodegenerative illnesses. Hawthorn (Crataegus oxyacantha) is a fruit-bearing shrub with a longstanding history as a medicinal agent. Currently, hawthorn is predominantly utilized for a range of pathological diseases. This research is designed to assess the neuroprotective impacts of exercise and hawthorn, both individually and together, on the hippocampus in the context of aging. Thirty male rats (24 old and six young) were allocated to six groups. In exercise groups, the animals underwent six weeks of treadmill exercise. Also, the treated rats with hawthorn extract received 100 mg/kg intraperitoneally. The open field and shuttle box tests were utilized to evaluate behavioral performance. Related kits measured the levels of MDA, SOD, and TNFα in the hippocampus. The western blotting method evaluated the protein expression of NFκB, COX2, and iNOS in the hippocampus. Also, the H&E, nissle, congo red, and tunnel stainings were utilized to investigate the hippocampus histology changes. Our results showed that following aging, the passive avoidance memory was impaired. Also, aging causes an increased level of oxidative stress and inflammation, as well as apoptosis and degeneration in the hippocampus tissue. However, HIIT and hawthorn extract could reduce inflammation and oxidative stress in the hippocampus. Also, the aging-induced histological changes were improved via HIIT and hawthorn extract administration.In conclusion, our findings revealed that six weeks of exercise and hawthorn extract can have neuroprotective effects following aging.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"137"},"PeriodicalIF":4.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144538014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bridging expectations and science: a roadmap for the future of longevity interventions.","authors":"Danyang Yu, Xinyi Zeng, David Barzilai, Dominik Thor, Yu-Xuan Lyu","doi":"10.1007/s10522-025-10278-z","DOIUrl":"10.1007/s10522-025-10278-z","url":null,"abstract":"<p><p>The field of longevity interventions has witnessed rapid expansion, driven by scientific advancements alongside growing industry and consumer interest. However, no longevity intervention has yet been proven effective or ready for widespread clinical adoption. A substantial gap persists between public expectations and the current scientific realities. This article explores four key themes: (1) consumer priorities regarding longevity interventions, (2) the type and depth of scientific information they value, (3) psychological, financial, and practical barriers limiting adoption, and (4) potential strategies to overcome these challenges. Despite increasing enthusiasm, clinical translation of longevity research is constrained by the lack of validated interventions, regulatory frameworks, and standardized biomarkers. By distinguishing between scientifically supported and unproven approaches, this article proposes a roadmap outlining the critical milestones necessary to advance longevity interventions from research to clinical readiness. The goal is to realign public understanding with the current state of longevity science and guide future efforts toward safe and effective translation.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"138"},"PeriodicalIF":4.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12213962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144538012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synbiotic supplementation enhances memory processes in adult and aged male rats.","authors":"Débora Aguirre Gonçalves, Jordana Griebler Luft, Manuel Adrian Riveros Escalona, Michele Bertoni Mann, Jeverson Frazzon, Márcio Dorn, Pabulo Henrique Rampelotto, Lucas de Oliveira Alvares","doi":"10.1007/s10522-025-10267-2","DOIUrl":"https://doi.org/10.1007/s10522-025-10267-2","url":null,"abstract":"<p><p>Synbiotic formulations, which combine prebiotics and probiotics in their composition, have shown promise in improving brain function and cognitive performance. However, the mechanisms by which synbiotics exert their beneficial effects on memory processes, particularly in the context of aging, remain unclear. In the present study, we investigated the effects of synbiotics supplementation on memory updating (reversal learning) and extinction in adult and aged rats. We also assessed the impact of the synbiotic intervention on the gut microbiota composition, diversity, and metabolism. The results showed that synbiotic supplementation (fructooligosaccharide and L. acidophilus, L. bulgaricius, L. casei, L. rhamnosus, and B. bifidum) improved memory updating in adult rats but not in aged rats. In contrast, the synbiotic facilitated memory extinction in aged rats, but not in adults. Interestingly, these cognitive benefits were not accompanied by significant alterations in the gut microbiome. This suggests that the synbiotic's effects on memory processes were mediated through more direct mechanisms, such as anti-inflammatory, antioxidant, and neuromodulatory actions, rather than through broad changes to the gut microbial community. These findings highlight the potential of synbiotic interventions to ameliorate age-related cognitive impairment and provide insights into the underlying mechanisms of the gut-brain axis.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"136"},"PeriodicalIF":4.4,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Translational potential of GADD45α: biomarker and therapeutic target in age-associated neurodegeneration and longevity.","authors":"Imran Kazmi, Fahad A Al-Abbasi, Mustafa Zeyadi, Misbahuddin Rafeeq, Alaa Hamed Habib, Johar Iqbal, Sami I Alzarea, Omar Awad Alsaidan, Muhammad Shahid Nadeem","doi":"10.1007/s10522-025-10277-0","DOIUrl":"https://doi.org/10.1007/s10522-025-10277-0","url":null,"abstract":"<p><p>Aging features a gradual decline in genomic integrity, epigenetic fidelity, and cellular homeostasis, driving the onset of chronic pathologies such as cancer, neurodegeneration, and metabolic disease. Growth arrest and DNA damage-inducible 45 alpha (GADD45α) functions as a pivotal stress-response mediator, coordinating DNA repair, cell-cycle arrest, oxidative stress defence, mitochondrial quality control, and chromatin remodeling. Researchers have extensively studied GADD45α in tumor suppression, but its roles in healthy aging and age-related disorders remain underexplored. Here, we provide a comprehensive synthesis of recent findings illuminating GADD45α's contributions to aging biology. We detail its engagement with nucleotide and base excision repair pathways to preserve genome stability, enforce G₂/M checkpoints to prevent damaged DNA propagation, and promote mitochondrial resilience under oxidative challenge. We then examine how GADD45α modulates epigenetic landscapes, mitigating age-associated DNA methylation drift and sustaining chromatin plasticity, and highlight its emerging neuroprotective actions in Alzheimer's and Parkinson's models. Integrating multi-omics analyses, in vivo rodent investigations, and Drosophila lifespan assays, we establish GADD45α as a dynamic biomarker of cellular aging and a promising geroprotective target. Finally, we discuss translational strategies to harness GADD45α activity, ranging from small-molecule enhancers and epigenetic modifiers to precision gene-editing to reinforce DNA repair capacity, delay senescence onset, and extend organismal healthspan. This review reframes GADD45α from a cancer-centric effector to a versatile regulator of aging processes, underscoring its therapeutic potential for promoting healthy longevity.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"135"},"PeriodicalIF":4.4,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The pro-aging and rejuvenating effects of young and aged perivascular adipose tissues on endothelial function and inflammation.","authors":"Chak Kwong Cheng, Xingtao Huang, Shuhui Meng, Yu Huang","doi":"10.1007/s10522-025-10283-2","DOIUrl":"https://doi.org/10.1007/s10522-025-10283-2","url":null,"abstract":"<p><p>Aging is considered as an independent risk factor for cardiovascular diseases. Common hallmarks of vascular aging include endothelial dysfunction, vascular inflammation, elevated oxidative stress, and telomere dysfunction. Perivascular adipose tissue (PVAT) is the local aggregate of adipose tissue surrounding the vascular bed, serving as a critical regulator of vascular function via either paracrine or endocrine manners. Aging-dependent malfunction of adipose tissues increases the risk of cardiometabolic diseases. Aging was previously shown to attenuate the anticontractile effect of PVAT in rodent arteries. Therefore, this study sought to understand whether aged and young PVAT promote and retard vascular aging in young and aged mice. PVAT-free aortas from aged and young mice were co-cultured with aortic PVAT from young and aged donor mice for 48 h, respectively. Endothelium-dependent relaxations (EDRs) in mouse aortas were determined by wire myography. Aged PVAT co-culture impaired endothelial function in the aortas of young mice, while young PVAT co-culture slightly alleviated endothelial dysfunction in aged mice. Aged PVAT co-culture induced vascular oxidative stress and inflammation, impaired telomere function, and suppressed AMPK/SIRT1 signaling in young mouse aortas. Conversely, these detrimental effects were partially reversed by young PVAT co-culture in aged mouse aortas. We further showed that these pro-aging and rejuvenating effects of PVAT were partially mediated by growth differentiation factor 15 (GDF15) and inflammatory cytokines. These findings highlight a substantial role of PVAT in modulating endothelial function and vascular aging, implying adipose-vascular axis as potential intervention target against cardiovascular aging and diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"134"},"PeriodicalIF":4.4,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of the Dicer family genes influences lifespan and stress resistance in a tissue-, sex-, and stressor-specific manner in Drosophila melanogaster.","authors":"Ekaterina Proshkina, Natalya Pakshina, Lyubov Koval, Evgeniya Shchegoleva, Nadezhda Zemskaya, Mikhail Shaposhnikov, Alexey Moskalev","doi":"10.1007/s10522-025-10272-5","DOIUrl":"https://doi.org/10.1007/s10522-025-10272-5","url":null,"abstract":"<p><p>Small non-coding RNAs coordinate essential cellular processes, including gene expression regulation, genome stability maintenance, and transposon suppression. These processes determine aging, lifespan, and resistance of cells and organisms to stress. In this work, we conducted a comprehensive study of the geroprotective effects of overexpression of two Dicer family genes (Dcr-1 and Dcr-2, which are responsible for the biogenesis of miRNAs and siRNAs) in different tissues of Drosophila melanogaster (nervous system, fat body, intestine, muscles). Activation of the Dicer genes affected the lifespan in a tissue- and sex-depending manner. Females with Dcr-1 overexpression in the nervous system exhibited a significant and reproducible increase in both median (10.0-13.4%, p < 0.001) and maximum lifespan (10.0-13.4%, p < 0.01). However, in other cases, the effect was insignificant or negative. Additionally, flies with neuronal Dcr-1 activation had increased expression of several longevity genes (Sirt1, bsk, tgo, Gadd45, Xpc, Azot, foxo, Hsf, Tsc1) and significantly increased survival after acute exposure to 700 Gy γ-radiation (40-200%, p < 0.05). But they had reduced resistance to starvation. This indicates a crucial role of the miRNA machinery and the Dicer family in providing protection against genotoxic effects and coordinating metabolic processes.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"130"},"PeriodicalIF":4.4,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Variety of sleep and circadian rhythms of elderly dementia patients living in group home residences.","authors":"Naoko Kubota, Noriko Matsuura, Maiko Ebina, Hitomi Suzuki, Nagomi Miyagi, Naoki Masukawa, Fumihiro Kouga, Yujiro Yamanaka","doi":"10.1007/s10522-025-10280-5","DOIUrl":"10.1007/s10522-025-10280-5","url":null,"abstract":"<p><p>In the present study, we investigated 70 elderly individuals with dementia residing in a group home in Japan (88.1 ± 6.6 SD years; 12 males and 58 females). Sleep measurements were collected via an accelerometer placed under the mattress from March 2021 to January 2024. The accelerometer-derived activity counts were transformed and plotted as actograms. On the basis of the actograms, sleep patterns were categorized into three groups: regular nighttime sleep (Type 1, n = 38, 54.3%), regular nighttime sleep with daytime naps (Type 2, n = 29, 41.4%), and irregular sleep (Type 3, n = 3, 4.3%). We compared accelerometer-derived sleep measures between the Type 1 and Type 2 groups due to the small number of participants in Type 3. Interestingly, Type 2 individuals had a significantly longer bed in time and total sleep time. However, their sleep onset latency, time of wakefulness after sleep onset and sleep efficiency did not differ from those of Type 1 individuals. Additionally, we assessed the relationships between sleep patterns and dementia characteristics, such as independence in daily living and level of care needed. No significant differences were observed in sleep measurements across these characteristics. To evaluate endogenous circadian rhythms, seven dementia patients (Type 1, n = 1; Type 2, n = 6) wore a patch-type wearable temperature sensor for approximately 24 h to estimate core body temperature (CBT). Although the zero-amplitude test revealed a significant rhythmicity in all patients, the CBT rhythms showed lower amplitude and unstable phases. In summary, our findings indicate that dementia patients display varying sleep patterns that are independent of dementia characteristics. The dysfunction of sleep homeostasis and entrainment of circadian pacemakers might be due to the light environment in the group home residence or impairment of the circadian clock itself in dementia patients.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"131"},"PeriodicalIF":4.4,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504800","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholesterol's hidden impact: the nonlinear link between remnant cholesterol (RC) and phenotypic age acceleration (PhenoAgeAccel).","authors":"QianKun Yang, Shan Zhu, YanFang Luo, HongBo Ai, Lei Feng, Li Zhang, Fei Luo","doi":"10.1007/s10522-025-10266-3","DOIUrl":"https://doi.org/10.1007/s10522-025-10266-3","url":null,"abstract":"<p><p>Cholesterol metabolism disorders have been shown to correlate with multiple physiopathologic aspects of cellular aging. However, whether indicators reflecting cholesterol metabolism [e.g., remnant cholesterol (RC)] can serve as biomarkers for biological aging remains unclear. To address this gap, this study aimed to explore the relationship between RC and phenotypic age acceleration (PhenoAgeAccel) using data from the National Health and Nutrition Examination Survey (NHANES) database. First, participants with complete information on RC, PhenoAgeAccel, and other essential covariates were included and analyzed. Subsequently, multivariable generalized linear regression models, subgroup analyses, interaction tests, and restricted cubic spline (RCS) analyses were utilized to explore the association. Results showed that a total of 4,471 participants were included for analysis. After adjusting for all potential covariates, a one-unit increase in RC was associated with a 0.724-year increase in PhenoAgeAccel (β = 0.724, 95% CI: 0.106-1.341). Notably, subgroup analyses and interaction tests further revealed a more pronounced RC-PhenoAgeAccel association in individuals with diabetes (β = 4.331, 95% CI: 1.607-7.055) and hypertension (β = 2.069, 95% CI: 0.887-3.251). In addition, RCS analysis identified a positive and nonlinear association between RC and PhenoAgeAccel (P for nonlinearity < 0.001), and threshold effect analysis determined an inflection point of 0.564 mmol/L for RC. Specifically, a positive and segmented RC-PhenoAgeAccel association was observed within the 0.564-mmol/L threshold (β = 9.653, 95% CI: 7.452-11.853), and such association remained significant beyond this point (β = 1.121, 95% CI: 0.193-2.049). In conclusion, RC was positively and nonlinearly associated with accelerated aging. Thus, controlling RC below 0.564 mmol/L might contribute to anti-aging effects and thereby help prevent aging-related diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"133"},"PeriodicalIF":4.4,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144511507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian clock and its effect on aging and lifespan.","authors":"Avnish Kumar Verma, Sandeep Singh, Syed Ibrahim Rizvi","doi":"10.1007/s10522-025-10281-4","DOIUrl":"https://doi.org/10.1007/s10522-025-10281-4","url":null,"abstract":"<p><p>The circadian clocks of the cell orchestrate a daily transcriptional rhythm that schedules key activities of the cell to maintain homeostasis and support resilience. Circadian rhythm is driven by the periodic oscillations of transcriptional activators and translational repressors, occurring in both the central and peripheral clocks. Accumulating evidence shows that aging impairs the functional synchrony of the circadian system which further escalate age-related disorders. In addition, the technological aspects of modern society, including constant work schedules and extensive use of personal electronics, have led to a significant rise in circadian disorders. Circadian dysfunction seems to adversely impact aging and longevity in animal models. Therefore, it is essential to conduct comprehensive studies to identify factors that worsen with aging and to discover therapeutic options for promoting healthy aging. This review examines how aging affects circadian function and the reciprocal effects of circadian disruption (CD) on aging and longevity. Further, we highlight the recent findings on non-pharmacological aspects such as dietary restrictions and physical exercise as a regulator of circadian rhythms, aging attenuation, and extending lifespan in mammals. Thus, resetting the circadian clock may lead to better synchrony in cellular homeodynamics and physiology which offers healthy aging and increased life span.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 4","pages":"132"},"PeriodicalIF":4.4,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}