ArticleAlcohol and alcoholism (Oxford, Oxfordshire)
Chronic ethanol consumption increases myocardial mitochondrial DNA mutations: a potential contribution by mitochondrial topoisomerases.
Article in Alcohol and alcoholism (Oxford, Oxfordshire). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026Review
- Article
- Giant mitochondria in cardiomyocytes: cellular architecture in health and disease.Basic research in cardiology · 2023Review
- NAD Supplement Alleviates Intestinal Barrier Injury Induced by Ethanol Via Protecting Epithelial Mitochondrial Function.Nutrients · 2022Article
- PDE5 inhibitor sildenafil attenuates cardiac microRNA 214 upregulation and pro-apoptotic signaling after chronic alcohol ingestion in mice.Molecular and cellular biochemistry · 2020Article
- Accelerated cardiomyocyte senescence contributes to late-onset doxorubicin-induced cardiotoxicity.American journal of physiology. Cell physiology · 2020Article
- Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis.The international journal of biochemistry & cell biology · 2017Review
- Mitochondrial fusion dynamics is robust in the heart and depends on calcium oscillations and contractile activity.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Alcoholic Myopathy: Pathophysiologic Mechanisms and Clinical Implications.Alcohol research : current reviews · 2017Review
- Alcohol's Effects on the Cardiovascular System.Alcohol research : current reviews · 2017Review
- Chronic plus binge ethanol feeding induces myocardial oxidative stress, mitochondrial and cardiovascular dysfunction, and steatosis.American journal of physiology. Heart and circulatory physiology · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
aimsAlcoholic cardiomyopathy (ACM) presents as decreased myocardial contractility, arrhythmias and secondary non-ischemic dilated cardiomyopathy leading to heart failure. Mitochondrial dysfunction is known to have a significant role in the development and complications of ACM. This study investigated if chronic ethanol feeding promoted myocardial mitochondrial topoisomerase dysfunction as one underlying cause of mitochondrial DNA (mtDNA) damage and mitochondrial dysfunction in ACM.
methodsThe impact of chronic ethanol exposure on the myocardial mitochondria was examined in both neonatal cardiomyocytes using 50 mM ethanol for 6 days and in rats assigned to control or ethanol feeding groups for 4 months.
resultsChronic ethanol feeding led to significant (P < 0.05) decreases in M-mode Fractional Shortening, ejection fraction, and the cardiac output index as well as increases in Tau. Ethanol feeding promoted mitochondrial dysfunction as evidenced by significantly decreased left ventricle cytochrome oxidase activity and decreases in mitochondrial protein content. Both in rats and in cultured cardiomyocytes, chronic ethanol presentation significantly increased mtDNA damage. Using isolated myocardial mitochondria, both mitochondrial topoisomerase-dependent DNA cleavage and DNA relaxation were significantly altered by ethanol feeding.
conclusionChronic ethanol feeding compromised cardiovascular and mitochondrial function as a result of a decline in mtDNA integrity that was in part the consequence of mitochondrial topoisomerase dysfunction. Understanding the regulation of the mitochondrial topoisomerases is critical for protection of mtDNA, not only for the management of alcoholic cardiomyopathy, but also for the many other clinical treatments that targets the topoisomerases in the alcoholic patient.
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