Cellular senescence and aging: molecular mechanisms and convergent pathways.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms and theoretical concepts with no primary data.
PubMed 42439909 · doi:10.1007/s00018-026-06317-8
What was done
The authors conducted a narrative review delineating the mechanistic overlaps and distinctions between cellular senescence (stress-induced stable cell-cycle arrest) and organismal aging (systemic functional decline). The review examines underlying triggers (DNA damage, telomere shortening, epigenetic changes, mitochondrial dysfunction), biomarkers, and therapeutic approaches including senolytics, partial reprogramming, and senescence-associated secretory phenotype (SASP) modulators.
What was found
The abstract reports no numerical findings or quantitative effect sizes. It qualitatively describes cellular senescence and aging as distinct but interconnected processes, detailing how senescent cell burden contributes to organismal decline and highlighting emerging intervention targets.
Why it matters
Clarifying the conceptual and biological differences between cellular-level senescence and organism-level aging helps standardize biomarker use and target discovery for age-related disease interventions.
Limits
As a narrative review, the paper presents no original empirical data, no systematic search methodology, and no quantitative synthesis of therapeutic efficacy.
Cited by
- supports Telomeres induce replicative senescence when they get too short, causing dividing cells to stop replicating.