Academic Journal

Assessing mechanisms and evidence of a causal role for cellular senescence and somatic mutations in aging.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Assessing mechanisms and evidence of a causal role for cellular senescence and somatic mutations in aging.
Συγγραφείς: Trastus LA; IFOM ETS - The AIRC Institute of Molecular Oncology, Milan 20139, Italy., d'Adda di Fagagna F; IFOM ETS - The AIRC Institute of Molecular Oncology, Milan 20139, Italy.; Istituto di Genetica Molecolare, Consiglio Nazionale delle Ricerche (IGM-CNR), Pavia 27100, Italy.
Πηγή: Aging [Aging (Albany NY)] 2026 Aug 26; Vol. 18 (1), pp. 1066-1076. Date of Electronic Publication: 2026 Aug 26.
Τύπος έκδοσης: Journal Article; Review
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Impact Journals, LLC Country of Publication: United States NLM ID: 101508617 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1945-4589 (Electronic) Linking ISSN: 19454589 NLM ISO Abbreviation: Aging (Albany NY) Subsets: MEDLINE
Imprint Name(s): Original Publication: Albany, NY : Impact Journals, LLC
Ιατρικοί όροι (MeSH): Cellular Senescence*/genetics , Cellular Senescence*/physiology , Aging*/genetics , Mutation*, Humans ; Animals ; DNA Damage ; Senescence-Associated Secretory Phenotype
Περίληψη: Understanding the primary molecular and cellular drivers of aging and how they trigger systemic functional decline remains a fundamental challenge. This review focuses on two proposed drivers of aging, cellular senescence and somatic DNA mutations, critically discusses the evidence for their association with organismal aging, and appraises their causal contribution to it. Several studies support the notion that cellular senescence can cause aging, acting through cell-intrinsic and, likely more significantly, cell-extrinsic mechanisms such as the senescence-associated secretory phenotype. Differently, the mutational burden is strongly correlated with aging, but we argue that the causal contribution of altered DNA sequences to age-related functional decline remains difficult to untangle from its originating genotoxic events.
Contributed Indexing: Keywords: DNA damage; SASP; aging; cellular senescence; somatic mutations
Entry Date(s): Date Created: 20260828 Date Completed: 20260828 Latest Revision: 20260828
Update Code: 20260829
DOI: 10.18632/aging.206414
PMID: 42664504
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1945-4589
DOI:10.18632/aging.206414