Beyond the Hayflick limit: How microbes influence cellular aging

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dc.contributor.authorAbavisani, Mohammad
dc.contributor.authorFaraji, Saba
dc.contributor.authorEbadpour, Negar
dc.contributor.authorKarav, Sercan
dc.contributor.authorSahebkar, Amirhossein
dc.date.accessioned2025-01-27T18:53:24Z
dc.date.available2025-01-27T18:53:24Z
dc.date.issued2025
dc.departmentÇanakkale Onsekiz Mart Üniversitesi
dc.description.abstractCellular 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 Pseudomonas aeruginosa and Helicobacter pylori introduce factors that damage host DNA or increase ROS, accelerating senescence via pathways such as NF-?B 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. © 2025 Elsevier B.V.
dc.identifier.doi10.1016/j.arr.2025.102657
dc.identifier.issn1568-1637
dc.identifier.scopus2-s2.0-85214337764
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.1016/j.arr.2025.102657
dc.identifier.urihttps://hdl.handle.net/20.500.12428/12701
dc.identifier.volume104
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherElsevier Ireland Ltd
dc.relation.ispartofAgeing Research Reviews
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_Scopus_20250125
dc.subjectAging; Cellular senescence; Microbiota; Oxidative stress
dc.titleBeyond the Hayflick limit: How microbes influence cellular aging
dc.typeReview Article

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