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Published on: May 25, 2017
[Alcoholic heart disease]
1National Research Center on Addictions, Malyy Mogil'tsevskiy per. 2, 119002 Moscow, Russia.
Insights
Alcoholic cardiomyopathy, a form of dilated cardiomyopathy, results from alcohol
Area of Science:
- Cardiology
- Toxicology
- Cell Biology
Context:
- Alcoholic cardiomyopathy is a significant health concern.
- Understanding its pathogenesis is crucial for effective treatment.
- This review synthesizes current knowledge on alcohol's impact on the heart.
Purpose:
- To review contemporary views on the pathogenesis of alcoholic cardiomyopathy.
- To elucidate the molecular and cellular mechanisms underlying alcohol-induced heart damage.
Summary:
- Alcohol's toxic effects on cardiomyocytes include apoptosis, organelle dysfunction, and calcium imbalance.
- Acetaldehyde, endocannabinoid system alterations, and lipid peroxidation contribute to myocardial injury.
- Key pathogenic mechanisms involve microperoxisome proliferation and hydrogen peroxide accumulation due to enzyme disbalance.
Impact:
- Provides a comprehensive overview of alcoholic cardiomyopathy pathogenesis.
- Highlights critical pathways for potential therapeutic interventions.
- Aids researchers and clinicians in understanding and managing this condition.
Abstract:
We present in this review contemporary views on pathogenesis of alcoholic cardiomyopathy. Alcoholic cardiomyopathy has features of dilated cardiomyopathy and is manifested by increased volume and hypertrophy of the left ventricle, diminished contractile capacity, and when decompensated - by lowering of cardiac output. Pathogenic action of alcohol on cardiomyocytes leads to activation of apoptosis, dysfunction of intracellular organelles, alterations of the system of myofilaments, disorder of intracellular homeostasis of calcium. Ethanol metabolite acetaldehyde, products of minor pathway of catecholamine metabolism, changes in the endocannabinoid system, and activation of processes of lipid peroxidation all contribute to the myocardial damage. The basis of pathogenesis of alcoholic cardiomyopathy constitute proliferation of microperoxisomes and disbalance between acyloxidase and catalase leading to accumulation of hydrogen peroxide inside myocytes.
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