Connecting autophagy to senescence in pathophysiology.
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.
Young
Andrew Rj
AR
Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Cambridge, CB2 0RE, United Kingdom.
Narita
Masashi
M
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
D047908:Intracellular Signaling Peptides and Proteins; C546842:MTOR protein, human; D017346:Protein Serine-Threonine Kinases; D058570:TOR Serine-Threonine Kinases; D001616:beta-Galactosidase