Senescence Can Be BETter without the SASP?

摘要

Global remodeling of the chromatin landscape occurs during senescence, although its functional consequence is still unclear. In this issue, Tasdemir and colleagues show that the epigenetic regulator BRD4 is required for expression of the proinflammatory senescence-associated secretory phenotype and immune clearance of senescent cells in vitro and in vivo. Their results could be useful in the design of novel therapies to treat aging-related diseases, including cancer. Cellular senescence is a stable arrest of cell proliferation triggered by replicative exhaustion or stresses such as DNA damage, oxidative stress, and aberrant oncogenic activation. In particular, oncogene-induced senescence (OIS) is important in tumor suppression, as numerous reports have demonstrated that it occurs in precancerous tissues in humans and mice and acts as a barrier to tumorigenesis. On the other hand, other modes of senescence are involved in embryonic and fetal development and wound healing, and accumulation of senescent cells in aged tissues promotes tissue aging (1). Baker and colleagues recently showed that the elimination from tissues of cells expressing a hallmark molecular marker of senescence, p16, promotes healthy aging (2).