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Cellular senescence is an evolutionarily selected physiological mechanism which is necessary during embryonic development and used later in life to limit tissue damage [1, 2]. In the short term, senescence is a protective response that limits tumorigenesis and aids wound healing. However, if senescent cells are not efficiently resolved by the immune system, they accumulate and, in the long term, may cause deleterious pathological consequences by promoting age-related diseases and cancer. In a recent study we demonstrated that senescent cells, induced to senesce via replicative exhaustion, oncogenic insult or DNA damage, upregulate proteins of the anti-apoptotic BCL-2 family in order to resist apoptosis [3]. Combined inhibition of these proteins using siRNAs or a small molecule ABT-737 induced selective death of senescent cells via apoptosis. The senolytic activity of ABT-737 molecule was demonstrated in two independent models of senescence in vivo. Importantly, clearance of senescent cells by ABT-737, as well as by its homolog compound ABT-263 in a different setting, resulted in increased proliferation of stem cells [3, 4]. This surprising effect of elimination of senescent cells might lead to improved tissue renewal and tissue fitness and thus contribute to lifespan extension.

mTOR signaling orchestrates the expression of cytoprotective factors during cellular senescence