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Summary
Cellular senescence is a state of “permanent” arrest of the cell division cycle. It is associated with hyperactivated secretion of proinflammatory factors and with a range of pathophysiological processes such as wound healing, aging, and cancer (1). The processes that control the senescence-associated secretory phenotype (SASP) are not well defined. One candidate effector mechanism is macroautophagy (herein referred to as autophagy), a major intracellular degradation system, but whether it promotes or inhibits senescence is disputed (2). On page 1503 of this issue, Kang et al. begin to unravel this paradox and provide new insights into the mechanisms by which the SASP is controlled (3).
