ArticleAutophagy2013
Multilevel regulation of autophagosome content by ethanol oxidation in HepG2 cells.
Article in Autophagy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
43 citing papers in PubMed, 66 citations in OpenAlex.
- Mechanism and regulation of mitophagy in liver diseases: a review.Frontiers in cell and developmental biology · 2025Review
- Plasma cathepsin D as an early indicator of alcohol-related liver disease.JHEP reports : innovation in hepatology · 2024Article
- Autophagy, Oxidative Stress, and Alcoholic Liver Disease: A Systematic Review and Potential Clinical Applications.Antioxidants (Basel, Switzerland) · 2023Review
- Ethanol Exposure to Ethanol-Oxidizing HEPG2 Cells Induces Intracellular Protein Aggregation.Cells · 2023Article
- Alcohol-Induced Lysosomal Damage and Suppression of Lysosome Biogenesis Contribute to Hepatotoxicity in HIV-Exposed Liver Cells.Biomolecules · 2021Article
- Autophagy of mucin granules contributes to resolution of airway mucous metaplasia.Scientific reports · 2021Article
- Rapid Identification of New Biomarkers for the Classification of GM1 Type 2 Gangliosidosis Using an UnbiasedCells · 2021Article
- Autophagy in liver diseases.World journal of hepatology · 2021Review
- Alcohol-and-HIV-Induced Lysosomal Dysfunction Regulates Extracellular Vesicles SecretionBiology · 2021Article
- Obeticholic acid attenuates human immunodeficiency virus/alcohol metabolism-induced pro-fibrotic activation in liver cells.World journal of hepatology · 2020Article
- Alcohol Metabolism Potentiates HIV-Induced Hepatotoxicity: Contribution to End-Stage Liver Disease.Biomolecules · 2019Article
- Autophagy, Metabolism, and Alcohol-Related Liver Disease: Novel Modulators and Functions.International journal of molecular sciences · 2019Review
- Hepatic NPC1L1 overexpression attenuates alcoholic autophagy in mice.Molecular medicine reports · 2019Article
- Diverse Consequences in Liver Injury in Mice with Different Autophagy Functional Status Treated with Alcohol.The American journal of pathology · 2019Article
- Ethanol withdrawal mitigates fatty liver by normalizing lipid catabolism.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Hepatic SIRT3 Upregulation in Response to Chronic Alcohol Consumption Contributes to Alcoholic Liver Disease in Mice.Frontiers in physiology · 2019Article
- Lipophagy and Alcohol-Induced Fatty Liver.Frontiers in pharmacology · 2019Review
- Ethanol and C2 ceramide activate fatty acid oxidation in human hepatoma cells.Scientific reports · 2018Article
- Chronic Alcohol Consumption Inhibits Autophagy and Promotes Apoptosis in the Liver.International journal of medical sciences · 2018Article
- Relevance of autophagy to fatty liver diseases and potential therapeutic applications.Amino acids · 2017Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Acute and chronic ethanol administration increase autophagic vacuole (i.e., autophagosome; AV) content in liver cells. This enhancement depends on ethanol oxidation. Here, we used parental (nonmetabolizing) and recombinant (ethanol-metabolizing) Hep G2 cells to identify the ethanol metabolite that causes AV enhancement by quantifying AVs or their marker protein, microtubule-associated protein 1 light chain 3-II (LC3-II). The ethanol-elicited rise in LC3-II was dependent on ethanol dose, was seen only in cells that expressed alcohol dehydrogenase (ADH) and was augmented in cells that coexpressed cytochrome CYP2E1 (P450 2E1). Furthermore, the rise in LC3-II was inversely related to a decline in proteasome activity. AV flux measurements and colocalization of AVs with lysosomes or their marker protein Lysosomal-Associated Membrane Protein 1 (LAMP1) in ethanol-metabolizing VL-17A cells (ADH (+) /CYP2E1 (+) ) revealed that ethanol exposure not only enhanced LC3-II synthesis but also decreased its degradation. Ethanol-induced accumulation of LC3-II in these cells was similar to that induced by the microtubule inhibitor, nocodazole. After we treated cells with either 4-methylpyrazole to block ethanol oxidation or GSH-EE to scavenge reactive species, there was no enhancement of LC3-II by ethanol. Furthermore, regardless of their ethanol-metabolizing capacity, direct exposure of cells to acetaldehyde enhanced LC3-II content. We conclude that both ADH-generated acetaldehyde and CYP2E1-generated primary and secondary oxidants caused LC3-II accumulation, which rose not only from enhanced AV biogenesis, but also from decreased LC3 degradation by the proteasome and by lysosomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.