Autophagy and Metabolism
- 3 December 2010
- journal article
- review article
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 330 (6009), 1344-1348
- https://doi.org/10.1126/science.1193497
Abstract
Autophagy is a process of self-cannibalization. Cells capture their own cytoplasm and organelles and consume them in lysosomes. The resulting breakdown products are inputs to cellular metabolism, through which they are used to generate energy and to build new proteins and membranes. Autophagy preserves the health of cells and tissues by replacing outdated and damaged cellular components with fresh ones. In starvation, it provides an internal source of nutrients for energy generation and, thus, survival. A powerful promoter of metabolic homeostasis at both the cellular and whole-animal level, autophagy prevents degenerative diseases. It does have a downside, however—cancer cells exploit it to survive in nutrient-poor tumors.Keywords
This publication has 37 references indexed in Scilit:
- PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1Nature, 2010
- Adipose-specific deletion of autophagy-related gene 7 ( atg7 ) in mice reveals a role in adipogenesisProceedings of the National Academy of Sciences of the United States of America, 2009
- Autophagy regulates adipose mass and differentiation in miceJCI Insight, 2009
- The Double-Edged Sword of Autophagy Modulation in CancerClinical Cancer Research, 2009
- The LKB1–AMPK pathway: metabolism and growth control in tumour suppressionNature Reviews Cancer, 2009
- Mitochondria-Anchored Receptor Atg32 Mediates Degradation of Mitochondria via Selective AutophagyDevelopmental Cell, 2009
- Atg32 Is a Mitochondrial Protein that Confers Selectivity during MitophagyDevelopmental Cell, 2009
- Autophagy Suppresses Tumorigenesis through Elimination of p62Cell, 2009
- Functional Significance and Morphological Characterization of Starvation-Induced Autophagy in the Adult HeartThe American Journal of Pathology, 2009
- Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesisCancer Cell, 2006