Cellular senescence — the state where cells permanently stop dividing but remain metabolically active — was first described in 1961. Over six decades, scientists transformed it from a curiosity into one of the most important mechanisms in aging biology. This review from the European Research Institute for the Biology of Aging traces that journey: from telomere shortening and tumor suppression to the discovery that senescent cells release a cocktail of inflammatory signals known as the SASP, which can damage surrounding tissue. Mouse studies later proved senescent cells directly drive age-related disease. Today, drugs called senolytics can selectively clear these cells, and early clinical trials are underway. Emerging single-cell technologies and precision biomarkers promise to make senescence research even more actionable in the near future.
