Although initially (in the 1960s) senescent cells appeared to be artefacts of culturing primary cells, by the 2000s they were discovered to accumulate in organs with age and during some disease processes. In addition to damaged DNA and halted proliferation, these cells exhibited the now famous proinflammatory trait named the senescence-associated secretory phenotype (SASP). In the 2010s, groundbreaking reports showed that eliminating senescent cells prolonged healthspan and improved disease outcomes in preclinical animal studies.

A landmark article by the Muñoz-Cánoves lab (Moiseeva et al., 2023) reported the first isolation of large numbers of senescent cells from old and injured skeletal muscles, leveraging the long-recognized marker senescence-associated β-galactosidase (SA-β-gal) activity to label and select senescent cells. This highly enriched population of senescent cells became extremely valuable material, informing the authors of specific ways in which senescent cells were detrimental for muscle regeneration; accordingly, eliminating senescent cells restored muscle function.