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PMID: 21127245 Published · ppublish English Journal Article Review

Autophagy and metabolism.

Science (New York, N.Y.) ·Vol. 330 ·No. 6009 ·2010-12-03 ·Pages 1344-8

Rabinowitz JD, White E

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 Autophagy preserves the health of cells and tissues by replacing outdated and damaged cellular components with fresh ones.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.

MeSH Terms
Animals Autophagy Cell Survival Disease Energy Metabolism Homeostasis Humans Metabolism Neoplasms/metabolism,pathology Phagosomes/metabolism Proteins/metabolism Signal Transduction Starvation TOR Serine-Threonine Kinases/metabolism
Chemicals
Proteins TOR Serine-Threonine Kinases
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Rabinowitz Joshua D
Department of Chemistry and Lewis-Sigler Institute for Integrative Genomics, 241 Carl Icahn Laboratory, Washington Road, Princeton University, Princeton, NJ 08544, USA. joshr@genomics.princeton.edu
White Eileen
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Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
1095-9203
Published
2010-12-03
Pages
1344-8
Language
English
Region
United States
NLM ID
0404511
PMCID
PMC3010857
Subset
IM
Grants
NCI NIH HHS · RC1 CA147961 · United States
NCI NIH HHS · RC1 CA147961-02 · United States
NCI NIH HHS · R37 CA053370-19 · United States
NCI NIH HHS · R01 CA130893 · United States
NCI NIH HHS · R01 CA130893-03 · United States
NCI NIH HHS · R37 CA053370 · United States
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