ArticleRedox biology2015
Chronic ethanol consumption induces mitochondrial protein acetylation and oxidative stress in the kidney.
Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 72 citations in OpenAlex.
- Crosstalk between cysteine and lysine modifications: Integrating redox and metabolic regulation.Redox biology · 2026Review
- Glyoxalase 1 loss reduces fatty liver but impairs glucose handling in male mice.Physiological reports · 2026Article
- Atmospheric stressors and kidney diseases.Nature reviews. Nephrology · 2026Review
- GCN5L1-Mediated Lysine Acetylation Regulates Mitochondrial Bioenergetics and Redox Homeostasis in the Aged Heart.Antioxidants (Basel, Switzerland) · 2026Article
- Timeless and Stainless Alcohol: Concentric Waves from Its Oxidative Metabolism and Related Oxidative Stress.Antioxidants (Basel, Switzerland) · 2026Review
- Mineralocorticoid receptors are implicated in the initial steps of the cardiorenal damage induced by ethanol.Frontiers in cardiovascular medicine · 2026Article
- The Link between Alcohol Consumption and Kidney Injury.The American journal of pathology · 2026Review
- Nephroprotective effects of ethanol leaf extract ofResearch in pharmaceutical sciences · 2025Article
- Class III Alcohol Dehydrogenase Modulates Renal Parietal Epithelial Cell Transformation During Chronic Alcohol Consumption in Mice.International journal of molecular sciences · 2025Article
- Alcohol- and Low-Iron Induced Changes in Antioxidant and Energy Metabolism Associated with Protein Lys Acetylation.International journal of molecular sciences · 2024Article
- Ambient ozone pollution impairs glucose homeostasis and contributes to renal function decline: Population-based evidence.Ecotoxicology and environmental safety · 2024Article
- Click chemistry-based thiol redox proteomics reveals significant cysteine reduction induced by chronic ethanol consumption.Redox biology · 2023Article
- Review
- Ameliorative Impacts of Wheat Germ Oil against Ethanol-Induced Hepatic and Renal Dysfunction in Rats: Involvement of Anti-Inflammatory, Anti-Apoptotic, and Antioxidant Signaling Pathways.Life (Basel, Switzerland) · 2022Article
- Proteomic analysis of alcohol-associated hepatitis reveals glycoprotein NMB (GPNMB) as a novel hepatic and serum biomarker.Alcohol (Fayetteville, N.Y.) · 2022Article
- Anti-Oxidant and Anti-Inflammatory Effects of Lipopolysaccharide fromMolecules (Basel, Switzerland) · 2021Article
- Sirtuin 3 regulates mitochondrial protein acetylation and metabolism in tubular epithelial cells during renal fibrosis.Cell death & disease · 2021Article
- Alcohol consumption and serum uric acid are synergistically associated with renal dysfunction among community-dwelling persons.Journal of clinical laboratory analysis · 2021Article
- Effect of alcohol consumption on kidney function: population-based cohort study.Scientific reports · 2021Article
- Effect of neuronal nitric oxide synthase serine-1412 phosphorylation on hypothalamic-pituitary-ovarian function and leptin response.Biology of reproduction · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
In this study, we present the novel findings that chronic ethanol consumption induces mitochondrial protein hyperacetylation in the kidney and correlates with significantly increased renal oxidative stress. A major proteomic footprint of alcoholic liver disease (ALD) is an increase in hepatic mitochondrial protein acetylation. Protein hyperacetylation has been shown to alter enzymatic function of numerous proteins and plays a role in regulating metabolic processes. Renal mitochondrial targets of hyperacetylation include numerous metabolic and antioxidant pathways, such as lipid metabolism, oxidative phosphorylation, and amino acid metabolism, as well as glutathione and thioredoxin pathways. Disruption of protein lysine acetylation has the potential to impair renal function through metabolic dysregulation and decreased antioxidant capacity. Due to a significant elevation in ethanol-mediated renal oxidative stress, we highlight the acetylation of superoxide dismutase, peroxiredoxins, glutathione reductase, and glutathione transferase enzymes. Since oxidative stress is a known factor in ethanol-induced nephrotoxicity, we examined biochemical markers of protein hyperacetylation and oxidative stress. Our results demonstrate increased protein acetylation concurrent with depleted glutathione, altered Cys redox potential, and the presence of 4-HNE protein modifications in our 6-week model of early-stage alcoholic nephrotoxicity. These findings support the hypothesis that ethanol metabolism causes an influx of mitochondrial metabolic substrate, resulting in mitochondrial protein hyperacetylation with the potential to impact mitochondrial metabolic and antioxidant processes.
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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.