Cellular aging is explained in part by two mechanistic hallmarks: mitochondrial dysfunction, formalized in the mitochondrial free radical theory of aging, which holds that reactive oxygen species generated as byproducts of oxidative cell respiration accumulate as damage over a cell's lifetime; and telomere attrition, the progressive shortening of the repetitive protective sequences at chromosome ends across successive somatic cell divisions. The free radical account has been refined by evidence that stress-induced mitochondrial biogenesis raises reactive oxygen species output simply by increasing mitochondrial number while also increasing energy yield, so the causal direction between reactive oxygen species and deterioration remains contested even though the association with aging is robust. Telomere attrition is bounded by the Hayflick limit — a finite replicative capacity for somatic cells lacking active telomerase, after which erosion extends into subtelomeric and genic regions; both mechanisms belong to cell biology and the physiology of senescence within the broader discipline of biology.
Cellular aging is explained in part by two mechanistic hallmarks: mitochondrial dysfunction, formalized in the mitochondrial free radical theory of aging, which holds that reactive oxygen species gen…