Ageing Research Reviews最新文献

{"title":"Insights into the toxic effects of micro-nano-plastics on the human brain and their relationship with the onset of neurological diseases: A narrative review","authors":"Carmela Rita Balistreri ,&nbsp;Daniele Magro ,&nbsp;Nafisa M. Jadavji","doi":"10.1016/j.arr.2025.102836","DOIUrl":"10.1016/j.arr.2025.102836","url":null,"abstract":"<div><div>The intensive production and use of plastics, poor biodegradability and inadequate recycling have caused excessive and alarming environmental pollution. This has led to the inevitable intake by humans, through different routes, of small plastic particles, the micro and nano-plastics (MNPs) with sizes ranging from nanometers (&lt;1000 nm) to micrometers (from 5 mm to 1 µm). MNPs can cause harmful effects in human tissues and organs, contributing to the early onset of aging and various age-related diseases. A growing body of evidence supports this toxic role of MNPs. In this regard, it has been shown that their different chemical and physical properties, including different chemical composition with different additives, different size, shape, solubility and ability to interact with metals and microbial agents, as well as the duration of multiple exposures, modulate their toxic action. In the brain, as documented mainly by studies conducted on brain tissues of deceased individuals, nanosized nanoparticles (NPs) of mostly 50 nm or smaller, made of polyethylene, bioaccumulate, causing damage. The mechanisms involved do not seem to be fully understood. However, studies on animal models and human cell cultures using plastic particles made of synthetic polystyrene, of slightly larger dimensions, partially clarify this aspect. They demonstrated that these particles have the unique ability to cross the blood-brain barrier and evoke neurotoxicity, through the activation of pathways that determine oxidative stress, inflammation, apoptosis, altered synthesis of neurotransmitters, endocrine molecules and key enzymes related to nerve conduction, and able to influence the gut-brain axis. Despite the paucity of studies conducted directly in humans, this review collects a growing body of evidence demonstrating that exposure to MNPs, and essentially NPs, can damage neurons. This could lead to alterations in learning, memory and behaviour, and could evoke additional potential negative impacts, contributing to amplifying neuroinflammation and the onset of neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases. Preventive approaches and measures to limit their use and human exposure, as well as potential therapeutic strategies, are also suggested.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102836"},"PeriodicalIF":12.5,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping the immune-genetic architecture of aging: A single-cell causal framework for biomarker discovery and therapeutic targeting","authors":"Yanggang Hong ,&nbsp;Yi Wang ,&nbsp;Wanyi Shu ,&nbsp;Jiajun Li ,&nbsp;Yuze Mi ,&nbsp;Haolin Chen ,&nbsp;Congde Chen","doi":"10.1016/j.arr.2025.102835","DOIUrl":"10.1016/j.arr.2025.102835","url":null,"abstract":"<div><div>Aging is a complex biological process driven by genetic and immune-mediated mechanisms, yet the causal roles of immune-cell-specific gene regulation remain unclear. In this study, we integrate single-cell expression quantitative trait loci (sc-eQTL) data with Mendelian randomization (MR) and colocalization analyses to identify immune-mediated regulatory mechanisms and therapeutic targets for aging. Using data from 14 immune cell types, we systematically evaluated 8733 eGenes for causal effects on telomere length (TL), facial aging (FA), and frailty index (FI). We identified 27 immune-cell-specific eGenes with significant causal associations and strong colocalization evidence (posterior probability for a shared causal variant, PP.H4 &gt; 50 %). Key regulators include FUBP1, TUFM, ATIC, and SLC22A5, with distinct effects across cell types and aging traits. Phenome-wide association studies (PheWAS) demonstrated minimal off-target associations for most genes, supporting their safety as therapeutic targets. Drug repurposing analysis revealed several approved or investigational compounds, such as Irofulven, zinc-based agents, and acetylcarnitine, with potential for aging-related interventions. Our findings provide new insights into the immune-genetic architecture of aging and establish a scalable framework for identifying cell-type-specific causal genes and repurposable drug targets. This approach enhances precision medicine strategies aimed at promoting healthy aging and delaying age-related decline.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102835"},"PeriodicalIF":12.5,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144638889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing rare neurological disorder diagnosis: Addressing challenges with systematic reviews and AI-driven MRI meta-trans learning framework for neurodegenerative disorders","authors":"Arshia Gupta,&nbsp;Deepti Malhotra","doi":"10.1016/j.arr.2025.102831","DOIUrl":"10.1016/j.arr.2025.102831","url":null,"abstract":"<div><div>Neurological Disorders (ND) affect a large portion of the global population, impacting the brain, spinal cord, and nerves. These disorders fall into categories such as NeuroDevelopmental (NDD), NeuroBiological (NBD), and NeuroDegenerative (ND_e) disorders, which range from common to rare conditions. While Artificial Intelligence (AI) has advanced healthcare diagnostics, training Machine Learning (ML) and Deep Learning (DL) models for early detection of rare neurological disorders remains a challenge due to limited patient data. This data scarcity poses a significant public health issue. Meta_Trans Learning (M_TAL), which integrates Meta-Learning (M_tL) and Transfer Learning (TL), offers a promising solution by leveraging small datasets to extract expert patterns, generalize findings, and reduce AI bias in healthcare. This research systematically reviews studies from 2018 to 2024 to explore how ML and M_TAL techniques are applied in diagnosing NDD, NBD, and ND_e disorders. It also provides statistical and parametric analysis of ML and DL methods for neurological disorder diagnosis. Lastly, the study introduces a MRI-based ND_e-M_TAL framework to aid healthcare professionals in early detection of rare neuro disorders, aiming to enhance diagnostic accuracy and advance healthcare practices.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102831"},"PeriodicalIF":12.5,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144614905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apheresis for senescence: Targeting the senescence-associated secretory phenotype to delay aging and age-related diseases","authors":"Yamac Akgun","doi":"10.1016/j.arr.2025.102832","DOIUrl":"10.1016/j.arr.2025.102832","url":null,"abstract":"<div><div>Aging is driven by cellular senescence and chronic inflammation, largely mediated by the senescence-associated secretory phenotype (SASP). SASP factors promote inflammaging, impair tissue homeostasis, and contribute to age-related diseases such as cardiovascular disease, neurodegeneration, and cancer. Current anti-aging strategies focus on senolytics or SASP inhibitors, yet these approaches have limitations. We discuss therapeutic plasma exchange (TPE) and selective apheresis, as interventions to mitigate SASP-driven aging. TPE removes inflammatory cytokines, metabolic waste, and senescence-associated proteins, while replenishing rejuvenating factors. Selective apheresis could enhance precision by targeting specific SASP components. By reducing systemic inflammation and restoring a youthful proteomic environment, these strategies may improve immune function, tissue regeneration, and overall healthspan. This review explores the mechanistic basis of SASP in aging and evaluates the potential of apheresis-based therapies as viable interventions to delay aging and age-related disease progression.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102832"},"PeriodicalIF":12.5,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144595926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding DNA repair regulation across human lifespan variability","authors":"Yunjia Tang,&nbsp;Dekai Zhang,&nbsp;Kaiyan Wang,&nbsp;Zhiyong Mao,&nbsp;Yu Chen","doi":"10.1016/j.arr.2025.102833","DOIUrl":"10.1016/j.arr.2025.102833","url":null,"abstract":"<div><div>DNA repair, an evolutionarily conserved mechanism essential for restoring genetic homeostasis, has been implicated in aging and longevity by multiple lines of evidence. However, due to the challenges in obtaining human research materials, studies on the interplay between DNA repair and aging rely primarily on laboratory animal models, whose regulatory mechanisms may not fully mirror those in humans. Strikingly, the rate of aging varies by nearly an order of magnitude across humans, ranging from individuals with progeroid syndromes (lifespans under a decade) to the longest-lived recorded person (122 years). This extreme diversity provides a unique framework for comparative analysis of lifespan regulation in humans. By integrating advances in DNA repair studies across humans with divergent aging trajectories, this review provides novel insights into the molecular basis of DNA repair and lifespan, highlighting promising targeted therapies to promote longevity through precise modulation of DNA repair pathways.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102833"},"PeriodicalIF":12.5,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144605754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Markers of biological age in dogs","authors":"Polina Zemko ,&nbsp;Marco Canevelli ,&nbsp;Sofia Pavanello ,&nbsp;Matteo Cesari ,&nbsp;Federico Bonsembiante ,&nbsp;Manuela Campisi ,&nbsp;Luana Cannella ,&nbsp;Simona Buscarnera ,&nbsp;Alessandro Zotti ,&nbsp;Tommaso Banzato","doi":"10.1016/j.arr.2025.102814","DOIUrl":"10.1016/j.arr.2025.102814","url":null,"abstract":"<div><div>As human life expectancy continues to rise, ageing and age-related diseases have become critical societal challenges, driving extensive research across genetics, molecular biology, biochemistry, and behavioral sciences. In this context, domestic dogs (<em>Canis lupus familiaris</em>) offer a unique model for ageing research due to their shared environmental exposures with humans, diverse genetic profiles, and relatively short lifespans. This review aims to identify potential biomarkers of ageing in dogs, facilitating a deeper understanding of age-related mechanisms and supporting the evaluation of interventions designed to promote healthy ageing. We present a research of peer-reviewed literature on age-related variations of various parameters across multiple biological systems, including epigenetic, telomere, immune, metabolic, and cognitive markers in dogs. Our findings highlight several robust biomarkers, such as DNA methylation-based epigenetic clocks, telomere attrition, CD4+/CD8+ T-cell ratio, hematological markers (e.g., globulin levels), and cognitive function scores. These biomarkers demonstrate strong parallels with human ageing processes, particularly concerning genomic and epigenetic alterations. However, challenges remain, including breed-specific variability, body size differences, and inconsistent evidence regarding inflammageing markers, such as pro-inflammatory cytokines. Despite these limitations, indicators of chronic inflammation (e.g., anemia of chronic disease and elevated globulins) are evident in older dogs. Future research directions include the standardization of biomarker protocols for dogs, the development of longitudinal studies to track dynamic age-related changes, and further exploration of emerging biomarkers, such as those related to microbiome composition and oxidative stress.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102814"},"PeriodicalIF":12.5,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144595925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of intratumoral microbiome in the occurrence, proliferation, metastasis of colorectal cancer and its underlying therapeutic strategies","authors":"Kaili Liao ,&nbsp;Jiarong Wen ,&nbsp;Ziqian Liu ,&nbsp;Beining Zhang ,&nbsp;Xue Zhang ,&nbsp;Yuxin Fu ,&nbsp;Wenyige Zhang ,&nbsp;Huan Hu ,&nbsp;Kun Ai ,&nbsp;Wenqing Zhu ,&nbsp;Meishi Xia ,&nbsp;Yixin Lai ,&nbsp;Yihui Qian ,&nbsp;Yanmei Xu ,&nbsp;Fan Sun ,&nbsp;Lei Zhang ,&nbsp;Qionghui Zhong ,&nbsp;Bo Huang ,&nbsp;Xiaozhong Wang","doi":"10.1016/j.arr.2025.102820","DOIUrl":"10.1016/j.arr.2025.102820","url":null,"abstract":"<div><div>Colorectal cancer (CRC), a leading cause of cancer mortality globally, is shaped by dynamic interactions between intratumoral microbiota and the tumor microenvironment (TME). Emerging evidence highlights the critical role of intratumoral bacteria, fungi, and viruses, such as <em>Fusobacterium nucleatum</em> and genotoxic <em>Escherichia coli</em>, in driving carcinogenesis through DNA damage, immune evasion, and metabolic reprogramming. While their origins remain debated, hypotheses include mucosal barrier penetration, migration from adjacent tissues, hematogenous dissemination, and co-metastasis with tumor cells. Spatial profiling reveals non-randomized microbial distribution within immunosuppressive TME niches characterized by reduced T-cell infiltration and enriched immunosuppressive molecules. Mechanistically, microbiota-derived metabolites (e.g., butyrate) and genotoxins (e.g., colibactin) modulate host pathways, promote epithelial DNA damage, polarize immune cells (e.g., M2-like macrophages, Tregs), and collectively, these contribute to fostering tumor progression. Conversely, microbial peptides or STING pathway activation by commensals like <em>Bifidobacterium</em> may enhance antitumor immunity. Intratumoral microbiota significantly influences therapeutic outcomes: <em>F. nucleatum</em> induces chemoresistance via autophagy, while <em>Gammaproteobacteria</em> inactivate gemcitabine. Immunotherapy responses are similarly modulated, with microbiota either amplifying antitumor T-cell activity or suppressing immunity through cytokine-mediated pathways. Innovative strategies, including engineered probiotics, bacterial vectors for drug delivery, and nanotechnology-enabled microbial modulation (e.g., functionalized nanoparticles, biomaterial carriers), aim to exploit these interactions. However, challenges such as low microbial biomass, contamination risks, and interpatient heterogeneity complicate translational efforts. Multi-omics and spatial-profiling technologies offer promise in deciphering microbial-immune-metabolic networks, guiding personalized therapies. Future research must address the biocompatibility of microbial-nanotech hybrids and validate intratumoral microbiota as biomarkers or therapeutic targets. Bridging gut and tumor microbiome studies could unlock novel CRC management strategies, emphasizing the dual role of microbiota as oncogenic drivers and therapeutic allies in precision oncology.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102820"},"PeriodicalIF":12.4,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144610524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics strategies to decode the molecular landscape of cellular senescence","authors":"Manuela Giovanna Basilicata ,&nbsp;Eduardo Sommella ,&nbsp;Lucia Scisciola ,&nbsp;Giovanni Tortorella ,&nbsp;Marco Malavolta ,&nbsp;Chiara Giordani ,&nbsp;Michelangela Barbieri ,&nbsp;Pietro Campiglia ,&nbsp;Giuseppe Paolisso","doi":"10.1016/j.arr.2025.102824","DOIUrl":"10.1016/j.arr.2025.102824","url":null,"abstract":"<div><div>Cellular senescence is a conserved cellular program characterized by a permanent cell cycle arrest triggered by a variety of stressors. Originally described as a tumor-suppressive mechanism, it is now recognized to exert pleiotropic and context-dependent functions, contributing to key physiological processes such as embryogenesis and tissue repair, as well as to processes associated with aging and the development of age-related diseases. Unlike normal cells, senescent cells remain metabolically active despite their non-dividing state. They significantly impact their environment through the Senescence-Associated Secretory Phenotype (SASP), a complex mix of cytokines, growth factors, and proteases. This secretory profile can promote tissue repair and regeneration but, if persistent, contributes to chronic inflammation, fibrosis, and tissue dysfunction. Two major pathways primarily regulate senescence: the p53/p21 and p16^INK4a^/Rb axes. These respond to stress signals like DNA damage, oxidative stress, and oncogenic activation, enforcing stable cell cycle arrest to prevent uncontrolled proliferation. However, as senescent cells accumulate over time, their ongoing SASP activity disrupts tissue homeostasis, driving inflammation and age-related diseases. Recent advances in multi-omics technologies, including metabolomics, proteomics, and lipidomics, have provided deeper insights into the complex molecular changes within senescent cells, revealing new biomarkers and potential therapeutic targets. These approaches offer a comprehensive understanding of cellular senescence, but challenges remain in distinguishing the causal relationships within these data and translating findings into clinical applications. This review integrates recent multi-omics discoveries, highlighting their potential to refine our understanding of senescence and support the development of targeted interventions to extend healthspan and combat age-related pathologies.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102824"},"PeriodicalIF":12.5,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144577182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The therapeutic potential of adiponectin and extracellular vesicles for promoting improved healthspan","authors":"Yubin Lei ,&nbsp;Hye Kyoung Sung ,&nbsp;Dylan Burger ,&nbsp;Gary Sweeney","doi":"10.1016/j.arr.2025.102823","DOIUrl":"10.1016/j.arr.2025.102823","url":null,"abstract":"<div><div>The gradual decline in physiological functions that comes with aging contributes to a range of chronic diseases, such as Alzheimer's, type 2 diabetes, heart failure, and osteoarthritis. Significant advancements in human longevity due to socioeconomic development have resulted in a foreseeable and substantial strain on the global healthcare system. In fact, there is now a shift in research focus towards enhancing healthspan. As a result, the development of improved therapies for various chronic diseases is essential to enhance healthspan in the aging population. Adiponectin, mainly produced in adipose tissue, is found at elevated levels in the blood of healthy centenarians. In contrast, lower circulating levels of adiponectin are inversely associated with the occurrence and severity of several age-related complications. Adiponectin plays a crucial role in promoting beneficial effects on key biological processes associated with aging-related diseases, contributing to improved healthspan and lifespan in preclinical models. In recent years, extracellular vesicles (EVs) have garnered significant research interest due to their crucial role in both local paracrine signaling and systemic inter-organ communication. They are now widely recognized for their potential as valuable diagnostic and therapeutic tools. In this review, we summarize current knowledge on the pathophysiological roles of adiponectin and EVs in aging, emphasizing their combined therapeutic potential in age-related diseases. Additionally, we explore the emerging evidence of crosstalk between adiponectin and EVs, underscoring their potential for developing improved strategies to promote healthy aging and longevity.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102823"},"PeriodicalIF":12.5,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144568208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms underlying the interplay between autophagy and the inflammasome in age-related diseases: Implications for exercise immunology","authors":"Eliézer Lucas Pires Ramos ,&nbsp;Ivo Vieira de Sousa Neto ,&nbsp;Ana Paula Pinto ,&nbsp;Dennys Esper Cintra ,&nbsp;Eduardo Rochete Ropelle ,&nbsp;José Rodrigo Pauli ,&nbsp;Ellen Cristini de Freitas ,&nbsp;Tiago Wilson Patriarca Mineo ,&nbsp;Adelino Sanchez Ramos da Silva","doi":"10.1016/j.arr.2025.102821","DOIUrl":"10.1016/j.arr.2025.102821","url":null,"abstract":"<div><div>Aging is a multifactorial process characterized by cellular dysfunction and increased susceptibility to age-related diseases. The interplay between autophagy and inflammasome has emerged as a critical factor influencing the aging process. Autophagy, which is responsible for degrading damaged cellular components, declines with age, leading to the accumulation of dysfunctional organelles and misfolded proteins. At the same time, the inflammasome, a key mediator of inflammatory responses, becomes hyperactivated in aging tissues, contributing to chronic low-grade inflammation, commonly referred to as \"inflammaging.\" This dysregulated interaction between autophagy and inflammasome activation plays a significant role in the development and progression of several age-related diseases. In cancer, reduced autophagic activity promotes tumorigenesis, while increased inflammasome activation establishes an inflammatory microenvironment that supports cancer progression. In arthritis, including both osteoarthritis and rheumatoid arthritis, impaired autophagy and inflammasome-driven inflammation contribute to joint degeneration. Neurodegenerative diseases such as Alzheimer's and Parkinson's are marked by defective autophagic clearance of protein aggregates and heightened inflammasome activation, leading to neuronal loss. Cardiovascular diseases, including atherosclerosis and myocardial dysfunction, also involve compromised autophagy and persistent inflammation, which accelerate vascular aging and cardiac damage. Exercise has emerged as a promising intervention for modulating the autophagy NLRP3 inflammasome axis. Moderate-intensity physical activity enhances autophagic flux by upregulating proteins such as BECLIN1, LC3, and ATG12, promoting mitochondrial quality control and reducing protein aggregates. This effect leads to decreased ROS production and suppression of NLRP3 inflammasome activation, lowering IL-1β and IL-18 levels, thereby helping to restore cellular homeostasis and reduce age-associated inflammation. Irisin also showed the importance of inhibiting inflammasome activation by promoting mitophagy after exercise. In both animal and human experiments, exercise has been shown to reduce systemic inflammation, improve cognitive function, attenuate joint degradation, and decrease cardiovascular risk, largely through these molecular pathways. This review explores recent findings that underscore the beneficial role of exercise in mitigating the effects of aging and preventing age-related diseases by regulating autophagy and inflammasome activities.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"110 ","pages":"Article 102821"},"PeriodicalIF":12.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}