Crosstalk between cellular senescence and selective autophagy

Coping with stress is essential for all organisms, and several stress responses have been evolved to maintain homeostasis. Autophagy and cellular senescence are two critical stress responses closely involved in aging and share a number of stimuli including telomere shortening, DNA damage, oncogenic stress and oxidative stress, suggesting their intimate relationship. Autophagy is originally thought to suppress cellular senescence by removing damaged macromolecules and organelles, yet recent studies also indicate that autophagy promotes cellular senescence by facilitating the synthesis of senescence-associated secretory proteins. These seemingly opposite roles of autophagy may reflect a complex picture of autophagy regulation on cellular senescence, including different types of autophagy or a unique spatiotemporal activation of autophagy. Thus, a better understanding of this complex relationship will provide therapeutic strategies for the treatment of many aging-related diseases and have important implications for human health. In this talk, I will discuss how selective autophagy shapes a program of cellular senescence including the senescence-associated secretory phenotype (SASP), a unique inflammatory response of senescent cells.