Autophagy as a stress-response and quality-control mechanism: implications for cell injury and human disease.
Autophagy, a vital catabolic process that degrades cytoplasmic components within the lysosome, is an essential cytoprotective response to pathologic stresses that occur during diseases such as cancer, ischemia, and infection. In addition to its role as a stress-response pathway, autophagy plays an essential quality-control function in the cell by promoting basal turnover of long-lived proteins and organelles, as well as by selectively degrading damaged cellular components. This homeostatic function protects against a wide variety of diseases, including neurodegeneration, myopathy, liver disease, and diabetes. This review discusses our current understanding of these two principal functions of autophagy and describes in detail how alterations in autophagy promote human disease.
Department of Pathology, Helen Diller Family Comprehensive Cancer Center, and Biomedical Sciences Graduate Program, University of California-San Francisco, CA 94143, USA. Lyndsay.Murrow@ucsf.edu
Lyndsay
L
Murrow
Jayanta
J
Debnath
D000818:Animals; D001343:Autophagy / Q000502:physiology*; D003424:Crohn Disease / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000473:pathology; D006801:Humans; D007239:Infections / Q000473:pathology; D008107:Liver Diseases / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000473:pathology; D019636:Neurodegenerative Diseases / Q000473:pathology; D013312:Stress, Physiological / Q000502:physiology*