Biogerontology最新文献

{"title":"From the lab to lifestyle: epigenetic clocks in personalized aging and health.","authors":"José Santiago Ibáñez-Cabellos, José Luis García-Giménez, Javier Escobar, Federico V Pallardó, Salvador Mena-Mollá","doi":"10.1007/s10522-026-10447-8","DOIUrl":"10.1007/s10522-026-10447-8","url":null,"abstract":"<p><p>Aging is a complex biological process characterized by progressive functional decline and increased risk of chronic diseases. In recent years, DNA methylation-based epigenetic clocks have emerged as some of the most robust biomarkers for estimating biological age. Initial research clocks, such as those developed by Horvath and Hannum, provided highly accurate chronological age predictions. Subsequent models, including PhenoAge, GrimAge, and DunedinPACE, improved upon this by incorporating health-related variables and functional measures, expanding their relevance to disease risk and pace of aging. Importantly, these multi-CpG clocks have demonstrated strong predictive accuracy, but their reliance on large numbers of CpG sites and high-throughput technologies limits their clinical scalability due to cost, complexity, and sample processing requirements. In this review, we critically evaluate the current landscape research-based epigenetic clocks, and their transition into direct-to-consumer testing. We discuss their key strengths, limitations, and translational potential, with particular emphasis on the growing demand for simplified, cost-effective, and analytically accessible epigenetic clocks, which should maintain predictive accuracy while enabling broader implementation in clinical and epidemiological settings. Special attention is given to ELOVL2-based clocks, which exemplify minimalistic yet robust models that can facilitate large-scale studies and democratize access to biological aging assessment. Ultimately, we argue that the next generation of epigenetic clocks should prioritize both analytical simplicity and validation across diverse populations to support personalized interventions for healthy aging.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833101","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":"Towards a context-aware framework for cellular senescence.","authors":"Arnab Nath, Parul Mehrotra, Chiranjib Bhattacharyya, Deepak Kumar Saini","doi":"10.1007/s10522-026-10440-1","DOIUrl":"https://doi.org/10.1007/s10522-026-10440-1","url":null,"abstract":"<p><p>From a cellular perspective, senescence has been considered a binary state, wherein cells are either senescent or not. This reductionist notion, often defined as irreversible growth arrest, has guided efforts to identify universal biomarkers and senolytics, but both have consistently eluded us. This outcome is not surprising, given that the biological nature of senescence may not be strictly irreversible; the accumulated evidence suggests that growth arrest can become unstable over time, with cells acquiring alterations, occasionally regaining proliferative capacity, or undergoing partial reprogramming, and exhibiting a heterogeneous spectrum of phenotypes (\"senotypes\") influenced by tissue types, stressors, temporal dynamics, and disease states. We propose that such a shift towards a dynamic spectrum of cellular states, is necessary to develop tailored strategies for context-specific signatures rather than a hypothetical state of cells that qualify for universal markers. The future of senescence research should thus focus on mapping, understanding, and utilising the spectrum of senescence states to mitigate its onset or modulate its progression.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833085","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 GHK-Cu delays aging in Caenorhabditis elegans via coordinated regulation of mitochondrial function and activation of DAF-16/SKN-1 pathways.","authors":"Huijun Wen, Keshu Zhao, Xiangjian Luo, Jian Pu, Yixin Li, Yi Dou, Jie He, Xinyu Nie, Yuan Ke, Wenhui Zhou","doi":"10.1007/s10522-026-10444-x","DOIUrl":"https://doi.org/10.1007/s10522-026-10444-x","url":null,"abstract":"<p><p>Aging is a complex biological process characterized by progressive functional decline across tissues and increased susceptibility to age-related diseases, with oxidative stress being a key contributing factor. Glycine-Histidine-Lysine (GHK), a naturally occurring tripeptide present in human plasma and urine, possesses potent antioxidant properties; however, its broader anti-aging potential remains inadequately explored. In this study, we employed the model organism Caenorhabditis elegans to systematically investigate the anti-aging effects of GHK-Cu (GHK complexed with copper) and elucidate its underlying molecular mechanisms. Our results demonstrated that GHK-Cu significantly extended lifespan of C. elegans and ameliorated mutiple aging-related phenotypes, including enhanced resistance to oxidative and thermal stress, improved motility, pharyngeal pumping, defecation rhythm, and reduced lipofuscin/lipid accumulation. Mechanistically, GHK-Cu preserved mitochondrial function by increasing mitochondrial membrane potential, alleviating age-related mitochondrial network fragmentation, shifting mitochondrial dynamics toward fusion via regulating drp-1 and fzo-1 expression, and promoting ATP biosynthesis. Meanwhile, GHK-Cu activating DAF-16 and SKN-1 pathway, and upregulating sod-3, gst-4, gcs-1, lys-7 and lys-8. This study provides the first mechanistic evidence that GHK-Cu delays aging through coordinated regulation of mitochondrial function and activation of both DAF-16 and SKN-1 pathways. Our findings identify novel molecular targets for developing anti-aging interventions and underscore the potential of GHK-Cu's as a multifaceted geroprotective compound.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833049","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":"Host genetics and diet jointly shape the microbiome of Drosophila melanogaster but do not predict lifespan or age-related traits.","authors":"Nikolaj Klausholt Bak, Stine Karstenskov Østergaard, Patrick Skov Schacksen, Jeppe Lund Nielsen, Palle Duun Rohde, Torsten Nygaard Kristensen","doi":"10.1007/s10522-026-10431-2","DOIUrl":"10.1007/s10522-026-10431-2","url":null,"abstract":"<p><p>The microbiome is a key determinant of organismal health, yet inter-individual variability and heterogeneous responses to environmental conditions complicates the understanding of its effects on hosts. Here, we present a comprehensive analysis using the Drosophila Genetic Reference Panel (DGRP) to investigate how the interplay between host genetic variation and diet influences microbiome composition, and to assess whether microbiome features in young flies can be used to predict lifespan and age-related traits. Our findings show that adult flies reared on a nutritionally rich control diet exhibited higher microbial richness but lower evenness compared to those on a nutritionally poor restricted diet. Principal component analysis (PCA) highlighted substantial diversity among lines reared on the same diet, and this variation was evidenced by high heritability estimates for all measured α-diversity metrics, including Unique OTU counts, Shannon and Simpson indices, as well as the relative abundances of genera and species with relative abundances exceeding 1%. These results underscore the critical roles of both environmental factors and genetic variation in shaping microbiome composition under different dietary conditions. Moreover, we identified widespread genotype-by-diet interactions, suggesting that the genetic regulation of the microbiome is highly complex. Finally, we found that the microbiome features of young flies including diversity indices, taxonomic abundances, or ordination scores cannot predict age-associated phenotypes (lifespan, locomotor activity, dry weight, and heat knockdown time). Our findings offer valuable insights into the genetic architecture that governs microbiome composition, dietary responses, and aging in Drosophila melanogaster.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13139259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810508","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":"Dissecting shared genetic architecture between pan-cancer and aging-related traits: a genome-wide cross-trait analysis.","authors":"Qiuyi Pu, Chao Wang, Xiaoxiao Mo, Lanlan Sha, Rui Zheng, Zhengdong Zhang, Dongmei Wu","doi":"10.1007/s10522-026-10446-9","DOIUrl":"https://doi.org/10.1007/s10522-026-10446-9","url":null,"abstract":"<p><p>The association between aging and cancer has been extensively documented in observational studies, but their shared genetic basis remains unclear. Leveraging genome-wide association studies summary statistics of aging and pan-cancer (87,531 cases and 314,193 controls) within the European population, genetic correlation and Mendelian randomization analyses were used to estimate genetic correlations, and infer causal relationships between seven aging-related traits and pan-cancer. We further conducted cross-trait and colocalization analyses to identify shared causal variants and then mapped them to genes. Differential expression analysis, RT-qPCR assays, enrichment analysis, and survival analysis were performed to explore the expression profiles of candidate genes and potential pathways. A significant negative genetic correlation between mvAge and pan-cancer was observed (r_g = -0.158, P = 7.41 × 10^-7). Concurrently, Mendelian randomization results supported a negative impact of pan-cancer on mvAge. We further identified five shared causal variants between mvAge and pan-cancer, and mapped them to five genes (CPA5, IRF4, KLHDC10, TYR, and ZC3HC1). High expression of ZC3HC1 was observed in bladder cancer tissues or bladder cancer cell lines, and was notably associated with low survival probability in bladder cancer. Enrichment analysis between high-ZC3HC1 and low-ZC3HC1 groups highlighted pathways related to chromosome separation and cell cycle. Our findings revealed a shared genetic basis linking aging and pan-cancer. We identified five causal variants in three colocalized loci and mapped them to five shared genes (CPA5, IRF4, KLHDC10, TYR, and ZC3HC1). In an exploratory downstream analysis, we observed that ZC3HC1 was differentially expressed in bladder cancer tissues, and high ZC3HC1 expression was associated with poorer survival outcomes.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810426","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":"Stress is inevitable; recovery is conditional: bioenergetic limits of resilience in aging and disease.","authors":"Torsak Tippairote, Pruettithada Hoonkaew, Aunchisa Suksawang, Prayfan Tippairote","doi":"10.1007/s10522-026-10445-w","DOIUrl":"https://doi.org/10.1007/s10522-026-10445-w","url":null,"abstract":"<p><p>Aging, stress-related disorders, and chronic disease are often examined across separate domains-stress physiology, nutrition, psychiatry, and geroscience-despite converging on shared phenotypes of functional decline and reduced resilience. Although adaptive responses to stress are well characterized, why comparable exposures yield sustained resilience in some individuals but progressive dysfunction in others remains insufficiently explained. We propose that the missing unifying constraint is not stress exposure itself, but the bioenergetic capacity to complete recovery. We reframe stress adaptation as a cyclical process comprising response, adaptation, and recovery, emphasizing that recovery is an active, ATP-dependent phase conditionally funded within a finite bioenergetic system. When mitochondrial processing capacity and redox flexibility are constrained, adaptive programs may persist beyond their functional window, contributing to mitochondrial congestion, epigenetic gridlock, and progressive loss of physiological plasticity-even in the absence of overt pathology. Within this perspective, we introduce Exposure-Related Malnutrition (ERM) as a proposed conceptual model describing a clinically interpretable and potentially reversible phenotype of unresolved bioenergetic triage. ERM is proposed to describe a state of relative undernutrition arising from chronic mismatch between energetic demand and recovery capacity, often occurring despite nominal intake and laboratory values within reference ranges. Distinct from frailty, sarcopenia, cachexia, metabolic syndrome, and classical malnutrition, ERM may reflect an upstream constraint in ATP-dependent recovery rather than structural loss, inflammatory wasting, metabolic thresholds, or inadequate intake. By integrating evolutionary allocation theory, developmental calibration, stress physiology, and mitochondrial mechanics, ERM is proposed to offer a unifying integrative framework for functional decline across aging and chronic disease. Clinically, this perspective shifts risk assessment from isolated thresholds toward coordinated biomarker patterns, trajectories, and recovery kinetics, potentially enabling recognition of vulnerability before incomplete resolution consolidates into irreversible pathology. We further outline translational implications of a recovery-centered approach, positioning mitochondrial processing capacity and intercellular bioenergetic support as modifiable determinants of long-term resilience.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810498","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 aging eye: navigating molecular mechanisms and innovative interventions.","authors":"Yumeng Lin, Zhongyu Han, Yunfeng Zhang, Ruimin Yuan, Mingyu Huang, Yating Liu, Jun Wang, Chen Xu, Luze Liu, Ping Yu, Qingsong Yang, Liuzhi Zeng, Sizhen Li","doi":"10.1007/s10522-026-10443-y","DOIUrl":"https://doi.org/10.1007/s10522-026-10443-y","url":null,"abstract":"<p><p>The global demographic shift toward aging has precipitated a surge in age-related ocular pathologies, imposing a formidable public health challenge that demands urgent intervention. Blinding disorders such as age-related macular degeneration (AMD), cataracts, and dry eye disease exemplify this crisis, with their pathogenesis being intrinsically linked to tissue-specific aging processes in the eye. At the molecular level, core pathways including telomere attrition, oxidative stress, cellular senescence, and autophagic dysregulation orchestrate this degenerative cascade. This review systematically delineates the dynamic interplay network of these pathways during ocular aging, with particular emphasis on four pivotal mechanisms: oxidative stress-driven reactive oxygen species (ROS) accumulation, senescence-associated secretory phenotype (SASP)-mediated inflammatory cascades, autophagic flux dysfunction, and epigenetic remodeling aberrations. We further evaluate recent advancements in translational therapies, emphasizing the clinical potential of targeted gene-editing technologies, stem cell-derived regenerative approaches, and novel senolytic agents. Additionally, artificial intelligence (AI) -assisted diagnostics are explored as pivotal tools for precision medicine, particularly in early disease detection via retinal imaging and biomarker analysis. Future research priorities should focus on the integration of aging-specific biomarkers including methylation signatures, the advancement of tissue-selective drug delivery systems tailored to anterior and posterior ocular compartments. Collectively, these initiatives will propel the development of targeted interventions to address age-related visual decline, positioning precision medicine as the cornerstone of next-generation geriatric ophthalmic care.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810480","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":"Pleiotropy and disease interactors: the dual nature of genes linking ageing and ageing-related diseases.","authors":"Gustavo Daniel Vega Magdaleno, João Pedro de Magalhães","doi":"10.1007/s10522-026-10429-w","DOIUrl":"10.1007/s10522-026-10429-w","url":null,"abstract":"<p><p>Ageing-related diseases (ARDs) display diverse phenotypes yet share an age-dependent rise in incidence, suggesting mechanistic links with ageing processes. We examined whether ageing-related genes differ systematically from genes associated with multiple ARD clusters. Across 57 ARDs from UK Biobank, network analyses showed that ageing-related genes, although rarely ARD-associated, lie significantly closer to many ARDs through greater-than-chance proximity in protein-protein interaction (PPI) and KEGG networks. Consistent with this network overlap, ageing-related genes tend to occupy intermediate tiers in KEGG signalling cascades and exhibit strong coexpression with disease-associated genes as well as low tissue specificity, supporting that they play regulatory roles across multiple tissues. In contrast, genes associated with multiple ARDs are enriched for immune disorders and tend to have fewer ARD-associated neighbors in PPI networks. Accordingly, genes associated with multiple ARDs also tend to be located in terminal branches of KEGG pathways and show high tissue specificity coupled with weak coexpression with other ARD genes. Lastly, machine learning integration based on gene-disease network topology identified candidate ageing-related genes enriched for intracellular signal transduction and programmed cell death. Altogether, this work reveals two genetic architectures of multi-ARD influence: a cross-tissue regulatory mechanism enriched in ageing-related genes, and a tissue-specific, immune-driven mechanism among pleiotropic disease-related genes.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761140","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":"Sirtuin 1 as an emerging exerkine in the aging process: unveiling its multifaceted biological roles.","authors":"Patrício Lopes de Araújo Leite, Larissa Alves Maciel, Rita Cristine Barboza Patricio, Geovanna Lopes Carneiro Pereira, Antônio Sérgio de Oliveira Lamounier, Samuel da Silva Aguiar, Caio Victor Sousa, Ivo Vieira de Sousa Neto, Herbert Gustavo Simões","doi":"10.1007/s10522-026-10442-z","DOIUrl":"10.1007/s10522-026-10442-z","url":null,"abstract":"<p><p>Sirtuin 1 (SIRT1) was initially identified as an enzyme that deacetylates histones and suppresses gene activity. Since then, its roles have expanded considerably, and it is now recognized as a multifunctional protein conserved across various organisms. Despite increasing interest, it remains essential to clarify how exercise-induced changes in SIRT1 counteract multiple hallmarks of aging, as well as the full scope of SIRT1's impact on different physiological systems. This review highlights recent findings on the short- and long-term effects of exercise on SIRT1 signaling in both rodents and humans during aging. We explore the molecular pathways activated in various tissues, providing insight into the specific biological functions of SIRT1 within aging cells. Optimal levels of SIRT1 help maintain homeostasis and a biochemical environment conducive to healthspan, influencing biological processes such as mitochondrial dynamics, metabolic pathways, tissue remodeling, autophagy, inflammatory responses, and redox balance. This indicates that SIRT1, a pleiotropic molecule, orchestrates multiple responses throughout aging. SIRT1 may act as a dynamic sensor for exercise benefits and protect against aging by maintaining genomic integrity. Different exercise protocols (acute and chronic) and modalities (aerobic, resistance, and combined training) can increase mRNA levels, activity, or protein levels of SIRT1 in various vital organs (adipose tissue, hippocampus, heart, liver, bone, and skeletal muscle) of aged animals and older adults, promoting health. Taken together, these observations support the notion that SIRT1 functions as a potential exerkine, and understanding its role in exercise-induced adaptations offers new insights into non-pharmacological strategies to enhance longevity.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761117","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":"Investigating fasting for metabolic health and longevity.","authors":"Matthew L Steinhauser, Pouneh K Fazeli","doi":"10.1007/s10522-026-10438-9","DOIUrl":"https://doi.org/10.1007/s10522-026-10438-9","url":null,"abstract":"<p><p>Humans have evolved adaptive mechanisms that enable survival even with zero calories for periods of months or longer. Intermittent 'low-dose' exposure to the metabolic stress of fasting may also activate pathways that promote metabolic health and longevity, although such benefits have not been proven in humans. Here we present our perspective of the current rationale and evidence base to support fasting for gain in metabolic health. In the absence of individual level risk factors for potential harm, such as frailty, osteoporosis or osteopenia, or a current/historical eating disorder, a trial of intermittent fasting or time-restricted eating to promote weight loss and metabolic health is reasonable for the motivated patient who is overweight or obese. We conclude, however, that the current state of evidence is limited and not sufficient to justify widespread adoption of fasting practices, nor is it sufficient to exclude the possibility that fasting holds a key to a longer life. We provide a template for the types of studies that will be required to optimize fasting protocols and establish therapeutic proof of concept. In our opinion, incorporation of mechanistic and multi-omics endpoints will be critical to understand potential mechanisms of benefit in humans; pathways that could ultimately be targeted with a fasting mimetic drug to obviate the need for long-term adherence to onerous dietary restriction.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 3","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761084","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}