Cellular senescence

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A stable arrest of cell division in which the cell remains metabolically active and secretes a characteristic mixture of inflammatory cytokines, proteases and growth factors known as the senescence-associated secretory phenotype. It is not simply cell death or exhaustion: it is a programme, triggered by telomere attrition, DNA damage, oncogene activation or other stress, and it is protective in the short term — it is one of the body's principal anti-cancer mechanisms and a component of wound healing. Its origins lie in Leonard Hayflick and Paul Moorhead's 1961 demonstration that normal human diploid fibroblasts divide only a limited number of times in culture, which refuted the then-prevailing belief that cells were intrinsically immortal. Senescent cells accumulate with age; in mice, genetically clearing them delays several age-related pathologies. Whether their accumulation is a cause of human ageing, a consequence of it, or both, is not settled, and no assay reliably counts senescent cells in a living human being.

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