ArticleScientific reports2016
NOX2 amplifies acetaldehyde-mediated cardiomyocyte mitochondrial dysfunction in alcoholic cardiomyopathy.
Article in Scientific reports, 2016. 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, 52 citations in OpenAlex.
- Alcohol Metabolism into Acetaldehyde in Developing Cerebral Arteries.International journal of molecular sciences · 2026Article
- Finerenone mitigates acute alcoholic myocardial injury by modulating inflammatory signaling, oxidative stress, and mitochondrial function.Molecular medicine (Cambridge, Mass.) · 2026Article
- E-cigarettes and cardiovascular health: a review of components, mechanisms, and clinical risk.American journal of cardiovascular disease · 2026Review
- Mineralocorticoid receptors are implicated in the initial steps of the cardiorenal damage induced by ethanol.Frontiers in cardiovascular medicine · 2026Article
- Tumor necrosis factor alpha triggers mitochondrial dysfunction and ROS-driven cytokine amplification in bovine fibroblast-like synoviocytes.Frontiers in veterinary science · 2026Article
- Neurotoxicity of Chronic Alcohol Exposure: Mechanistic Insights, Cellular Disruption, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Alcoholic cardiomyopathy: an update.European heart journal · 2024Review
- Electronic cigarettes and cardiovascular disease: epidemiological and biological links.Pflugers Archiv : European journal of physiology · 2024Review
- Global, regional and national burden of alcohol cardiomyopathy from Global Burden of Disease Study 2019.Internal and emergency medicine · 2023Article
- The Generation of Nitric Oxide from Aldehyde Dehydrogenase-2: The Role of Dietary Nitrates and Their Implication in Cardiovascular Disease Management.International journal of molecular sciences · 2022Review
- Review
- Myocardial Injury Caused by Chronic Alcohol Exposure-A Pilot Study Based on Proteomics.Molecules (Basel, Switzerland) · 2022Article
- Acetaldehyde Induces Cytotoxicity via Triggering Mitochondrial Dysfunction and Overactive Mitophagy.Molecular neurobiology · 2022Article
- Losartan protects human stem cell-derived cardiomyocytes from angiotensin II-induced alcoholic cardiotoxicity.Cell death discovery · 2022Article
- Inhibition of (Pro)renin Receptor-Mediated Oxidative Stress Alleviates Doxorubicin-Induced Heart Failure.Frontiers in oncology · 2022Article
- Alcohol Use Disorders and Their Harmful Effects on the Contractility of Skeletal, Cardiac and Smooth Muscles.Advances in drug and alcohol research · 2021Article
- Oxidative Stress and Hypertension.Circulation research · 2021Review
- Proteomic Profiling Reveals Roles of Stress Response, CaAlcoholism, clinical and experimental research · 2020Article
- NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein.Antioxidants (Basel, Switzerland) · 2020Article
- Investigating the Vascular Toxicity Outcomes of the Irreversible Proteasome Inhibitor Carfilzomib.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alcoholic cardiomyopathy (ACM) resulting from excess alcohol consumption is an important cause of heart failure (HF). Although it is assumed that the cardiotoxicity of the ethanol (EtOH)-metabolite acetaldehyde (ACA) is central for its development and progression, the exact mechanisms remain obscure. Murine cardiomyocytes (CMs) exposed to ACA or EtOH showed increased superoxide (O2(•-)) levels and decreased mitochondrial polarization, both being normalized by NADPH oxidase (NOX) inhibition. C57BL/6 mice and mice deficient for the ACA-degrading enzyme mitochondrial aldehyde dehydrogenase (ALDH-2(-/-)) were fed a 2% EtOH diet for 5 weeks creating an ACA-overload. 2% EtOH-fed ALDH-2(-/-) mice exhibited a decreased cardiac function, increased heart-to-body and lung-to-body weight ratios, increased cardiac levels of the lipid peroxidation product malondialdehyde (MDA) as well as increased NOX activity and NOX2/glycoprotein 91(phox) (NOX2/gp91(phox)) subunit expression compared to 2% EtOH-fed C57BL/6 mice. Echocardiography revealed that ALDH-2(-/-)/gp91(phox-/-) mice were protected from ACA-overload-induced HF after 5 weeks of 2% EtOH-diet, demonstrating that NOX2-derived O2(•-) contributes to the development of ACM. Translated to human pathophysiology, we found increased gp91(phox) expression in endomyocardial biopsies of ACM patients. In conclusion, ACM is promoted by ACA-driven mitochondrial dysfunction and can be improved by ablation of NOX2/gp91(phox). NOX2/gp91(phox) therefore might be a potential pharmacological target to treat ACM.
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