Cellular senescence is a fate-determined state in response to stress, involving diverse effector mechanisms, such as autophagy activation, epigenetic and high-order chromatin structure alterations and activation of a secretory program. Through the senescence-associated secretory phenotype (SASP), senescent cells actively communicate with their surroundings and the immune system, having a profound impact on the tissue microenvironment. This is a dynamic and progressive process; the timely control of the SASP and senescence resolution is critical for tissue homeostasis. I will introduce the view that the proper execution of a senescence lifecycle is critical for the physiological role of senescence, whereas senescence-associated pathologies may be a consequence of a deviation from an intact senescence lifecycle (see our recent review PMID 30709901 ). Underlying mechanisms of senescence functionality (or the SASP ), with emphasis on epigenetics and autophagy, will be discussed.
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