Ageing Research Reviews最新文献

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Beyond amyloid plaque, targeting α-synuclein in Alzheimer disease: The battle continues
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-04 DOI: 10.1016/j.arr.2025.102684
Hayder M. Al-kuraishy , Ghassan M. Sulaiman , Hamdoon A. Mohammed , Ali I. Al-Gareeb , Ali K. Albuhadily , Amer Al Ali , Mohammed H. Abu-Alghayth
{"title":"Beyond amyloid plaque, targeting α-synuclein in Alzheimer disease: The battle continues","authors":"Hayder M. Al-kuraishy ,&nbsp;Ghassan M. Sulaiman ,&nbsp;Hamdoon A. Mohammed ,&nbsp;Ali I. Al-Gareeb ,&nbsp;Ali K. Albuhadily ,&nbsp;Amer Al Ali ,&nbsp;Mohammed H. Abu-Alghayth","doi":"10.1016/j.arr.2025.102684","DOIUrl":"10.1016/j.arr.2025.102684","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is the most common neurodegenerative brain disease and represents the most frequent type of dementia characterized by cognitive impairment and amnesia. AD neuropathology is connected to the development of synaptic dysfunction and loss of synaptic homeostasis due to an imbalance in the production and clearance of β-amyloid (Aβ) and intracellular neurofibrillary tangles (NFTs). However, AD neuropathology is complex and may relate to the deposition of other misfolded proteins, such as alpha-synuclein (α-Syn). Of note, α-Syn, which is involved in the pathogenesis of Parkinson disease (PD) and Lewy body (LB) dementia, is also implicated in AD neuropathology. However, the potential role of α-Syn in AD neuropathology is elusive. Therefore, this review aims to discuss the pathological role of α-Syn in AD and how targeting α-Syn aggregates may be effective in treating AD.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"105 ","pages":"Article 102684"},"PeriodicalIF":12.5,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143308088","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}
引用次数: 0
Validation requirements for AI-based intervention-evaluation in aging and longevity research and practice 基于人工智能的老龄化与长寿研究与实践干预评估的验证要求
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-01 DOI: 10.1016/j.arr.2024.102617
Georg Fuellen , Anton Kulaga , Sebastian Lobentanzer , Maximilian Unfried , Roberto A. Avelar , Daniel Palmer , Brian K. Kennedy
{"title":"Validation requirements for AI-based intervention-evaluation in aging and longevity research and practice","authors":"Georg Fuellen ,&nbsp;Anton Kulaga ,&nbsp;Sebastian Lobentanzer ,&nbsp;Maximilian Unfried ,&nbsp;Roberto A. Avelar ,&nbsp;Daniel Palmer ,&nbsp;Brian K. Kennedy","doi":"10.1016/j.arr.2024.102617","DOIUrl":"10.1016/j.arr.2024.102617","url":null,"abstract":"<div><div>The field of aging and longevity research is overwhelmed by vast amounts of data, calling for the use of Artificial Intelligence (AI), including Large Language Models (LLMs), for the evaluation of geroprotective interventions. Such evaluations should be correct, useful, comprehensive, explainable, and they should consider causality, interdisciplinarity, adherence to standards, longitudinal data and known aging biology. In particular, comprehensive analyses should go beyond comparing data based on canonical biomedical databases, suggesting the use of AI to interpret changes in biomarkers and outcomes. Our requirements motivate the use of LLMs with Knowledge Graphs and dedicated workflows employing, e.g., Retrieval-Augmented Generation. While naive trust in the responses of AI tools can cause harm, adding our requirements to LLM queries can improve response quality, calling for benchmarking efforts and justifying the informed use of LLMs for advice on longevity interventions.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102617"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Oxidative stress and mitochondrial impairment: Key drivers in neurodegenerative disorders
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-01 DOI: 10.1016/j.arr.2025.102667
Pei Wen, Zhixin Sun, Fengting Gou, Jingjing Wang, Qing Fan, Deming Zhao, Lifeng Yang
{"title":"Oxidative stress and mitochondrial impairment: Key drivers in neurodegenerative disorders","authors":"Pei Wen,&nbsp;Zhixin Sun,&nbsp;Fengting Gou,&nbsp;Jingjing Wang,&nbsp;Qing Fan,&nbsp;Deming Zhao,&nbsp;Lifeng Yang","doi":"10.1016/j.arr.2025.102667","DOIUrl":"10.1016/j.arr.2025.102667","url":null,"abstract":"<div><div>Mitochondrial dysfunction and oxidative stress are critical factors in the pathogenesis of neurodegenerative diseases. The complex interplay between these factors exacerbates neuronal damage and accelerates disease progression. In neurodegenerative diseases, mitochondrial dysfunction impairs ATP production and promotes the generation of reactive oxygen species (ROS). The accumulation of ROS further damages mitochondrial DNA, proteins, and lipids, creating a vicious cycle of oxidative stress and mitochondrial impairment. This review aims to elucidate the mechanisms by which mitochondrial dysfunction and oxidative stress lead to neurodegeneration, and to highlight potential therapeutic targets to mitigate their harmful effects.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102667"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029891","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}
引用次数: 0
The cross-talk between the cGAS-STING signaling pathway and chronic inflammation in the development of musculoskeletal disorders cGAS-STING信号通路与慢性炎症在肌肉骨骼疾病发展中的串扰。
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-01 DOI: 10.1016/j.arr.2024.102602
Alexander Kalinkovich , Gregory Livshits
{"title":"The cross-talk between the cGAS-STING signaling pathway and chronic inflammation in the development of musculoskeletal disorders","authors":"Alexander Kalinkovich ,&nbsp;Gregory Livshits","doi":"10.1016/j.arr.2024.102602","DOIUrl":"10.1016/j.arr.2024.102602","url":null,"abstract":"<div><div>Musculoskeletal disorders (MSDs) comprise diverse conditions affecting bones, joints, and muscles, leading to pain and loss of function, and are one of the most prevalent and major global health concerns. One of the hallmarks of MSDs is DNA damage. Once accumulated in the cytoplasm, the damaged DNA is sensed by the cyclic GMP-AMP synthase (cGAS)/stimulator of interferon genes (STING) pathway, which triggers the induction of type I interferons and inflammatory cytokines. Thus, this pathway connects the musculoskeletal and immune systems. Inhibitors of cGAS or STING have shown promising therapeutic effects in the pre-clinical models of several MSDs. Systemic, chronic, low-grade inflammation (SCLGI) underlies the development and maintenance of many MSDs. Failure to resolve SCLGI has been hypothesized to play a critical role in the development of chronic diseases, suggesting that the successful resolution of SCLGI will result in the alleviation of their related symptomatology. The process of inflammation resolution is feasible by specialized pro-resolving mediators (SPMs), which are enzymatically generated from dietary essential polyunsaturated fatty acids (PUFAs). The supplementation of SPMs or their stable, small-molecule mimetics and receptor agonists has revealed beneficial effects in inflammation-related animal models, including arthropathies, osteoporosis, and muscle dystrophy, suggesting a translational potential in MSDs. In this review, we substantiate the hypothesis that the use of cGAS-STING signaling pathway inhibitors together with SCLG-resolving compounds may serve as a promising new therapeutic approach for MSDs.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102602"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755960","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}
引用次数: 0
An overview of the genes and biomarkers in Alzheimer’s disease 阿尔茨海默病的基因和生物标志物综述。
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-01 DOI: 10.1016/j.arr.2024.102599
Hari Krishnan Krishnamurthy , Vasanth Jayaraman , Karthik Krishna , Tianhao Wang , Kang Bei , Chithra Changalath , John J. Rajasekaran
{"title":"An overview of the genes and biomarkers in Alzheimer’s disease","authors":"Hari Krishnan Krishnamurthy ,&nbsp;Vasanth Jayaraman ,&nbsp;Karthik Krishna ,&nbsp;Tianhao Wang ,&nbsp;Kang Bei ,&nbsp;Chithra Changalath ,&nbsp;John J. Rajasekaran","doi":"10.1016/j.arr.2024.102599","DOIUrl":"10.1016/j.arr.2024.102599","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is the most common type of dementia and neurodegenerative disease characterized by neurofibrillary tangles (NFTs) and amyloid plaque. Familial AD is caused by mutations in the <em>APP, PSEN1</em>, and <em>PSEN2</em> genes and these mutations result in the early onset of the disease. Sporadic AD usually affects older adults over the age of 65 years and is, therefore classified as late-onset AD (LOAD). Several risk factors associated with LOAD including the <em>APOE</em> gene have been identified. Moreover, GWAS studies have identified a wide array of genes and polymorphisms that are associated with LOAD risk. Currently, the diagnosis of AD involves the evaluation of memory and personality changes, cognitive impairment, and medical and family history to rule out other diseases. Laboratory tests to assess the biomarkers in the body fluids as well as MRI, CT, and PET scans to analyze the presence of plaques and NFTs are also included in the diagnosis of AD. It is important to diagnose AD before the onset of clinical symptoms, i.e. during the preclinical stage, to delay the progression and for better management of the disease. Research has been conducted to identify biomarkers of AD in the CSF, serum, saliva, and urine during the preclinical stage. Current research has identified several biomarkers and potential biomarkers in the body fluids that enhance diagnostic accuracy. Aside from genetics, other factors such as diet, physical activity, and lifestyle factors may influence the risk of developing AD. Clinical trials are underway to find potential biomarkers, diagnostic measures, and treatments for AD mainly in the preclinical stage. This review provides an overview of the genes and biomarkers of AD.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102599"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142756015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Targeted microbiota dysbiosis repair: An important approach to health management after spinal cord injury 靶向微生物群失调修复:脊髓损伤后健康管理的重要途径。
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-01 DOI: 10.1016/j.arr.2024.102648
Cheng Ju , Renfeng Liu , Yanming Ma , Hui Dong , Ruiqing Xu , Huimin Hu , Dingjun Hao
{"title":"Targeted microbiota dysbiosis repair: An important approach to health management after spinal cord injury","authors":"Cheng Ju ,&nbsp;Renfeng Liu ,&nbsp;Yanming Ma ,&nbsp;Hui Dong ,&nbsp;Ruiqing Xu ,&nbsp;Huimin Hu ,&nbsp;Dingjun Hao","doi":"10.1016/j.arr.2024.102648","DOIUrl":"10.1016/j.arr.2024.102648","url":null,"abstract":"<div><div>Current research primarily focuses on the pathological mechanisms of spinal cord injury (SCI), seeking to promote spinal cord repair and restore motorial and sensory functions by elucidating mechanisms of cell death or axonal regeneration. However, SCI is almost irreversible, and patients often struggle to regain mobility or self-care abilities after injuries. Consequently, there has been significant interest in modulating systemic symptoms following SCI to improve patients' quality of life. Neuron axonal disconnection and substantial apoptotic events following SCI result in signal transmission loss, profoundly impacting various organ and systems, including the gastrointestinal tract. Dysbiosis can lead to severe bowel dysfunction in patients, substantially lowering their quality of life and significantly reducing life expectancy of them. Therefore, researches focusing on the restoration of the gut microbiota hold promise for potential therapeutic strategies aimed at rehabilitation after SCI. In this paper, we explore the regulatory roles that dietary fiber, short-chain fatty acids (SCFAs), probiotics, and microbiota transplantation play in patients with SCI, summarize the potential mechanisms of post-SCI dysbiosis, and discuss possible strategies to enhance long-term survival of SCI patients. We aim to provide potential insights for future research aimed at ameliorating dysbiosis in SCI patients.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102648"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901070","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}
引用次数: 0
The role and mechanism of triptolide, a potential new DMARD, in the treatment of rheumatoid arthritis 雷公藤甲素在类风湿关节炎治疗中的作用及机制。
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-01 DOI: 10.1016/j.arr.2024.102643
Xiwen Wang, Tianyang Ni, Jianru Miao, Xinyao Huang, Zhe Feng
{"title":"The role and mechanism of triptolide, a potential new DMARD, in the treatment of rheumatoid arthritis","authors":"Xiwen Wang,&nbsp;Tianyang Ni,&nbsp;Jianru Miao,&nbsp;Xinyao Huang,&nbsp;Zhe Feng","doi":"10.1016/j.arr.2024.102643","DOIUrl":"10.1016/j.arr.2024.102643","url":null,"abstract":"<div><div>Triptolide (TP) is the primary pharmacological component of Tripterygium Glycosides (TG), which has anti-inflammatory, antiproliferative, and immunosuppressive properties, among other pharmacological actions, and has excellent potential for developing into a new DMARD. We have reviewed the effects and mechanisms of TP on immunosuppression, inhibiting synovial proliferation, and preventing articular bone destruction in the treatment of rheumatoid arthritis (RA), which is a common disease in the elderly in this paper. We have found that TP has regulatory effects on multiple vital cells in the above-mentioned pathological process of RA, such as monocytes/macrophages, dendritic cells, T cells, fibroblast-like synoviocytes, and osteoclasts. We also found that TP can regulate multiple key signaling pathways such as NF-κB, JAK/STAT, and MAPK through various molecular regulatory mechanisms, achieving regulatory effects on numerous phenotypes of the above-mentioned vital cells.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102643"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901071","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}
引用次数: 0
The immunosenescence clock: A new method for evaluating biological age and predicting mortality risk 免疫衰老时钟:评估生物年龄和预测死亡风险的新方法。
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-01 DOI: 10.1016/j.arr.2024.102653
Shuyu Li , Ke Wang , Jingni Wu , Yongliang Zhu
{"title":"The immunosenescence clock: A new method for evaluating biological age and predicting mortality risk","authors":"Shuyu Li ,&nbsp;Ke Wang ,&nbsp;Jingni Wu ,&nbsp;Yongliang Zhu","doi":"10.1016/j.arr.2024.102653","DOIUrl":"10.1016/j.arr.2024.102653","url":null,"abstract":"<div><div>Precisely assessing an individual's immune age is critical for developing targeted aging interventions. Although traditional methods for evaluating biological age, such as the use of cellular senescence markers and physiological indicators, have been widely applied, these methods inherently struggle to capture the full complexity of biological aging. We propose the concept of an 'immunosenescence clock' that evaluates immune system changes on the basis of changes in immune cell abundance and omics data (including transcriptome and proteome data), providing a complementary indicator for understanding age-related physiological transformations. Rather than claiming to definitively measure biological age, this approach can be divided into a biological age prediction clock and a mortality prediction clock. The main function of the biological age prediction clock is to reflect the physiological state through the transcriptome data of peripheral blood mononuclear cells (PBMCs), whereas the mortality prediction clock emphasizes the ability to identify people at high risk of mortality and disease. We hereby present nearly all of the immunosenescence clocks developed to date, as well as their functional differences. Critically, we explicitly acknowledge that no single diagnostic test can exhaustively capture the intricate changes associated with biological aging. Furthermore, as these biological functions are based on the acceleration or delay of immunosenescence, we also summarize the factors that accelerate immunosenescence and the methods for delaying it. A deep understanding of the regulatory mechanisms of immunosenescence can help establish more accurate immune-age models, providing support for personalized longevity interventions and improving quality of life in old age.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102653"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142923869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Roles of SIRT3 in cardiovascular and neurodegenerative diseases SIRT3在心血管和神经退行性疾病中的作用。
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-01 DOI: 10.1016/j.arr.2024.102654
Yu Cheng , Anqi Zhao , Ying Li , Cheng Li , Xiao Miao , Wanshan Yang , Yonggang Wang
{"title":"Roles of SIRT3 in cardiovascular and neurodegenerative diseases","authors":"Yu Cheng ,&nbsp;Anqi Zhao ,&nbsp;Ying Li ,&nbsp;Cheng Li ,&nbsp;Xiao Miao ,&nbsp;Wanshan Yang ,&nbsp;Yonggang Wang","doi":"10.1016/j.arr.2024.102654","DOIUrl":"10.1016/j.arr.2024.102654","url":null,"abstract":"<div><div>Sirtuin-3 (SIRT3) in mitochondria has nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase activity. As such, SIRT3 is crucial in cardiovascular and neurodegenerative diseases. Advanced proteomics and transcriptomics studies have revealed that SIRT3 expression becomes altered when the heart or brain is affected by external stimuli or disease, such as diabetic cardiomyopathy, atherosclerosis, myocardial infarction, Alzheimer's disease, Huntington's disease, and Parkinson's disease. More specifically, SIRT3 participates in the development of these disorders through its deacetylase activity and in combination with downstream signaling pathways. The paper reviews SIRT3’s expression changes, roles, and mechanisms associated with the development of cardiovascular and neurodegenerative diseases. Additionally, strategies targeting SIRT3 to treat or regulate cardiovascular and neurodegenerative disease development are discussed.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102654"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928260","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}
引用次数: 0
Beyond the Hayflick limit: How microbes influence cellular aging 超越海弗利克极限:微生物如何影响细胞衰老。
IF 12.5 1区 医学
Ageing Research Reviews Pub Date : 2025-02-01 DOI: 10.1016/j.arr.2025.102657
Mohammad Abavisani , Saba Faraji , Negar Ebadpour , Sercan Karav , Amirhossein Sahebkar
{"title":"Beyond the Hayflick limit: How microbes influence cellular aging","authors":"Mohammad Abavisani ,&nbsp;Saba Faraji ,&nbsp;Negar Ebadpour ,&nbsp;Sercan Karav ,&nbsp;Amirhossein Sahebkar","doi":"10.1016/j.arr.2025.102657","DOIUrl":"10.1016/j.arr.2025.102657","url":null,"abstract":"<div><div>Cellular senescence, a complex biological process resulting in permanent cell-cycle arrest, is central to aging and age-related diseases. A key concept in understanding cellular senescence is the Hayflick Limit, which refers to the limited capacity of normal human cells to divide, after which they become senescent. Senescent cells (SC) accumulate with age, releasing pro-inflammatory and tissue-remodeling factors collectively known as the senescence-associated secretory phenotype (SASP). The causes of senescence are multifaceted, including telomere attrition, oxidative stress, and genotoxic damage, and they extend to influences from microbial sources. Research increasingly emphasizes the role of the microbiome, especially gut microbiota (GM), in modulating host senescence processes. Beneficial microbial metabolites, such as short-chain fatty acids (SCFAs), support host health by maintaining antioxidant defenses and reducing inflammation, potentially mitigating senescence onset. Conversely, pathogenic bacteria like <em>Pseudomonas aeruginosa</em> and <em>Helicobacter pylori</em> introduce factors that damage host DNA or increase ROS, accelerating senescence via pathways such as NF-κB and p53-p21. This review explores the impact of bacterial factors on cellular senescence, highlighting the role of specific bacterial toxins in promoting senescence. Additionally, it discusses how dysbiosis and the loss of beneficial microbial species further contribute to age-related cellular deterioration. Modulating the gut microbiome to delay cellular senescence opens a path toward targeted anti-aging strategies. This work underscores the need for deeper investigation into microbial influence on aging, supporting innovative interventions to manage and potentially reverse cellular senescence.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102657"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960202","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}
引用次数: 0
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