Cocaine elicits autophagic cytotoxicity via a nitric oxide-GAPDH signaling cascade
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Significance: Cocaine is one of the most abused drugs in modern society, with overdoses that are frequently lethal. Molecular mechanisms underlying its toxic actions have been obscure. The present study demonstrates that cocaine’s cellular toxicity involves a signaling cascade that utilizes the gasotransmitter nitric oxide, which leads to autophagy, a cellular modification that can cause cell death. Thus, manipulations that impair nitric oxide signaling and autophagy diminish cytotoxic actions of cocaine. By contrast, alterations of apoptosis and other nonautophagic modes of cell death are ineffective. Therapies directed toward the autophagic process may be beneficial in treating cocaine neurotoxicity.
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Abolishing autophagy pharmacologically or by depleting ATG5 or BECN1 prevents cocaine neurotoxicity in cultured neurons.
“Along similar lines, abolishing autophagy by pharmacological means or by genetically depleting ATG5 or BECN1, prevents the neurotoxicity of cocaine in cultured neurons [848].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [848]
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- Authors
- Guha, P., Harraz, M. M., & Snyder, S. H.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Snyder, Solomon H.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2016-01-19
- Volume
- 113
- Issue
- 5
- Pages
- 1417-1422
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC4747760
- OpenAlex
- W2253617369
- Cited by
- 70
- References
- 51
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 2 · 2023: 8 · 2022: 5 · 2021: 11 · 2020: 6 · 2019: 8 · 2018: 10 · 2017: 7 · 2016: 7
- FWCI
- 9.99
- Type
- journal article
- Language
- en
- Update notices
- correction (2017-02-27)
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Johns Hopkins University
- National Institutes of Health (DA-000266)
- National Institute on Drug Abuse (P50DA000266, DA000266)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Forensic Toxicology and Drug Analysis
- Keywords
- cocaine, autophagy, autophagic cell death, nitric oxide, glyceraldehyde-3-phosphate dehydrogenase, parthanatos, necroptosis, apoptosis, neurotoxicity, LC3-II, p62, ATG5, Beclin-1, PARP1, RIPK1, cocaine overdose
- MeSH terms
- Animals, Autophagy, Cells, Cultured, Cocaine, Glyceraldehyde-3-Phosphate Dehydrogenases, Humans, Nitric Oxide, Signal Transduction, Mice
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