Senescence is the progressive decline in biological function that accompanies aging, observable both as organismal aging and, at the cellular level, as cellular senescence, a state of stable, irreversible growth arrest in which cells cease to divide while remaining metabolically active. Cellular senescence is trigge…
Senescence is the progressive decline in biological function that accompanies aging, observable both as organismal aging and, at the cellular level, as cellular senescence, a state of stable, irreversible growth arrest in which cells cease to divide while remaining metabolically active. Cellular senescence is triggered by telomere attrition, oxidative and genotoxic stress, and oncogenic or replicative signals, and it serves dual roles: it can suppress tumor formation by halting the proliferation of damaged cells, as seen when disturbed cell-cycle regulation induces premature senescence and limits tumor growth, yet the accumulation of senescent cells also contributes to tissue dysfunction and aging. Mechanistically, senescence is linked to oxidative damage and the role of nutritional antioxidants in telomere maintenance, to telomerase activity whose inhibition accelerates aging, and to molecular pathways and regulatory factors, including signaling axes and microRNAs, that govern the regenerative capacity of stem and satellite cells. Senescence intersects with age-related and degenerative disease, immune decline and frailty, and the impaired self-renewal of tissues, and it is increasingly studied as a target for interventions that aim to delay aging or restore regenerative function. By connecting molecular damage, cell-cycle control, and tissue maintenance to the broader process of growing old, senescence is central to the biology of aging, cancer, and regeneration.
9 peer-reviewed articles, ranked by relevance. Each links to its DOI.
The 9 articles above have been cited 31 times in the scholarly literature. Citation data via OpenAlex and Crossref, updated Jun 2026.
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