Autophagy and Metabolism
Open accessAbstract
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 Autophagy preserves the health of cells and tissues by replacing outdated and damaged cellular components with fresh ones.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.
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Glutamine metabolism plays a critical role in tumor progression by supporting mitochondrial oxidative phosphorylation, supplying TCA cycle intermediates, glutathione synthesis, NEAA synthesis, and producing NADPH.
“Unsurprisingly, glutamine metabolism plays a critical role in tumor progression since it not only supports mitochondrial oxidative phosphorylation but also supplies metabolic intermediates for the TCA cycle, glutathione synthesis, and NEAA synthesis and simultaneously produces NADPH157–159.”
From Glutamine reliance in cell metabolism (2020) · cites this paper as [159]
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- Authors
- Rabinowitz, J. D., & White, E.
- Affiliations
- Princeton University (US)
- Rutgers, The State University of New Jersey (US)
- Venue
- Science
- Published
- 2010-12-03
- Volume
- 330
- Issue
- 6009
- Pages
- 1344-1348
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3010857
- OpenAlex
- W2039607936
- Cited by
- 1,982
- References
- 37
- Citations by year
- 2026: 54 · 2025: 82 · 2024: 97 · 2023: 110 · 2022: 165 · 2021: 175 · 2020: 172 · 2019: 128 · 2018: 108 · 2017: 144 · 2016: 143 · 2015: 132 · 2014: 123 · 2013: 151 · 2012: 120
- FWCI
- 12.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R37CA053370, RC1CA147961, R01CA130893)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- autophagy, cellular metabolism, lysosomal degradation, metabolic homeostasis, starvation, energy production, degenerative diseases, cancer cells
- MeSH terms
- Animals, Autophagy, Cell Survival, Disease, Energy Metabolism, Homeostasis, Humans, Metabolism, Neoplasms, Phagosomes, Proteins, Starvation, Signal Transduction, TOR Serine-Threonine Kinases
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