title: Connecting autophagy to senescence in pathophysiology.
abstract: Cellular senescence is an extremely stable form of cell cycle arrest activated in response to stress. Autophagy, a lysosome-dependent cellular catabolic process, can also be triggered by cellular stresses. Both senescence and autophagy have been implicated in a similar range of pathophysiologies, including cancer, aging and age-related symptoms. Senescence is a heterogeneous phenotype that is composed of multiple effector mechanisms and autophagy was recently identified as a new effector of senescence. Autophagy seemingly has different impacts on cells responding to stress through a diversity of effects: recycling of metabolic waste, cell survival and protein expression regulation.
authors.affiliation: Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge, CB2 0RE, United Kingdom.
authors.forename: Andrew Rj
authors.initials: AR
authors.lastname: Young
authors.forename: Masashi
authors.initials: M
authors.lastname: Narita
mesh_terms: D000818:Animals; D001343:Autophagy; D016922:Cellular Senescence; D004194:Disease; D025461:Feedback, Physiological; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D010641:Phenotype; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases; D001616:beta-Galactosidase / Q000378:metabolism
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; C546842:MTOR protein, human; D017346:Protein Serine-Threonine Kinases; D058570:TOR Serine-Threonine Kinases; D001616:beta-Galactosidase