title: Autophagic defects in aging: looking for an "emergency exit"?
abstract: The ability of cells to renew their intracellular components and get rid of undesired or altered molecules decreases with age. Failure of autophagy is considered one of the main reasons for the build up of damaged components in the tissues of old organisms. We have recently shown that, declined activity of chaperone-mediated autophagy, a selective type of autophagy particularly impaired in aging, increases cell's vulnerability to stressors. This finding supports that, added to its role in cellular clean up, chaperone-mediated autophagy is an essential component of the cellular response to stress. Failure to perform this function with age could underlie the inability of old cells to adapt to stress conditions, and explain the accelerated course of some protein conformational disorders, such as Parkinson's disease, as affected individuals age.
authors.affiliation: Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, New York, USA.
authors.forename: Ashish C
authors.initials: AC
authors.lastname: Massey
authors.forename: Roberta
authors.initials: R
authors.lastname: Kiffin
authors.forename: Ana Maria
authors.initials: AM
authors.lastname: Cuervo
mesh_terms: D000818:Animals; D001343:Autophagy; D016922:Cellular Senescence / Q000502:physiology*; D006801:Humans; D018832:Molecular Chaperones / Q000378:metabolism; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D018832:Molecular Chaperones; D046988:Proteasome Endopeptidase Complex