ReviewRedox biology2014
Ethanol-induced oxidant stress modulates hepatic autophagy and proteasome activity.
Review in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 52 citations in OpenAlex.
- Alcohol Metabolism into Acetaldehyde in Developing Cerebral Arteries.International journal of molecular sciences · 2026Article
- Enhanced CaNature communications · 2023Article
- Multiomics Approach Captures Hepatic Metabolic Network Altered by Chronic Ethanol Administration.Biology · 2022Article
- Downregulating PDPK1 and taking phillyrin as PDPK1-targeting drug protect hepatocytes from alcoholic steatohepatitis by promoting autophagy.Cell death & disease · 2022Article
- Novel Insights into Alcoholic Liver Disease: Iron Overload, Iron Sensing and Hemolysis.Journal of translational internal medicine · 2022Article
- Therapeutic regulation of autophagy in hepatic metabolism.Acta pharmaceutica Sinica. B · 2022Review
- Autophagy in liver diseases: A review.Molecular aspects of medicine · 2021Review
- Moderate chronic ethanol consumption exerts beneficial effects on nonalcoholic fatty liver in mice fed a high-fat diet: possible role of higher formation of triglycerides enriched in monounsaturated fatty acids.European journal of nutrition · 2020Article
- Autophagy, Metabolism, and Alcohol-Related Liver Disease: Novel Modulators and Functions.International journal of molecular sciences · 2019Review
- Alcohol abuse and disorder of granulopoiesis.Pharmacology & therapeutics · 2019Review
- Ethanol withdrawal mitigates fatty liver by normalizing lipid catabolism.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Redox regulation of proteasome function.Redox biology · 2017Review
- Oxidation-Responsive, EuACS omega · 2017Article
- Mystic Acetaldehyde: The Never-Ending Story on Alcoholism.Frontiers in behavioral neuroscience · 2017Review
- p62/SQSTM1-Dr. Jekyll and Mr. Hyde that prevents oxidative stress but promotes liver cancer.FEBS letters · 2016Review
- Evaluation of Eu(II) -based positive contrast enhancement after intravenous, intraperitoneal, and subcutaneous injections.Contrast media & molecular imaging · 2016Article
- Heme oxygenase-1 alleviates alcoholic liver steatosis: histopathological study.Journal of toxicologic pathology · 2016Article
- A Mechanistic Review of Mitophagy and Its Role in Protection against Alcoholic Liver Disease.Biomolecules · 2015Review
- Alcohol and Viral Hepatitis: Role of Lipid Rafts.Alcohol research : current reviews · 2015Review
- Diallyl Sulfide: Potential Use in Novel Therapeutic Interventions in Alcohol, Drugs, and Disease Mediated Cellular Toxicity by Targeting Cytochrome P450 2E1.Current drug metabolism · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In this review, we describe research findings on the effects of alcohol exposure on two major catabolic systems in liver cells: the ubiquitin-proteasome system (UPS) and autophagy. These hydrolytic systems are not unique to liver cells; they exist in all eukaryotic tissues and cells. However, because the liver is the principal site of ethanol metabolism, it sustains the greatest damage from heavy drinking. Thus, the focus of this review is to specifically describe how ethanol oxidation modulates the activities of the UPS and autophagy and the mechanisms by which these changes contribute to the pathogenesis of alcohol-induced liver injury. Here, we describe the history and the importance of cellular hydrolytic systems, followed by a description of each catabolic pathway and the differential modulation of each by ethanol exposure. Overall, the evidence for an involvement of these catabolic systems in the pathogenesis of alcoholic liver disease is quite strong. It underscores their importance, not only as effective means of cellular recycling and eventual energy generation, but also as essential components of cellular defense.
Indexed as
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What OpenQuestion holds
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.