A "radical" mitochondrial view of autophagy-related pathology
Year: 2009
Type: article
Abstract: Copyright: © Raimundo and Shadel. This is an open‐access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Autophagy is a critical catabolic process through which cytoplasmic components are degraded, with the primary purpose of removing long-lived and/or damaged proteins and organelles and recycling essential anabolic building-block molecules [1]. Mechanistically, this involves formation of autophagosomes that are fused with lysosomes to facilitate digestion of the internalized components by lysosomal proteases. Proteins that mediate specific steps of the autophagy pathway have been characterized, mutations in which cause severe disease pathology affecting tissues such as muscle, brain, heart, liver and the immune system [2]. In
Source: Aging
Authors: Nuno Raimundo, Gerald S. Shadel
Institution: Yale University
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W1703425354