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Int. J. Mol. Sci. 2016, 17(10), 1651;

New Treatment Strategies for Alcohol-Induced Heart Damage

Alcohol Unit, Department of Internal Medicine, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain
Departament of Biochemistry and Molecular Biomedicine, Faculty of Biology, Avda Diagonal 643, Universitat de Barcelona, 08028 Barcelona, Spain
Author to whom correspondence should be addressed.
Academic Editor: Ashok K. Singh
Received: 27 June 2016 / Revised: 15 September 2016 / Accepted: 16 September 2016 / Published: 29 September 2016
(This article belongs to the Special Issue Alcoholism: Molecular Mechanisms and Treatment Strategies)
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High-dose alcohol misuse induces multiple noxious cardiac effects, including myocyte hypertrophy and necrosis, interstitial fibrosis, decreased ventricular contraction and ventricle enlargement. These effects produce diastolic and systolic ventricular dysfunction leading to congestive heart failure, arrhythmias and an increased death rate. There are multiple, dose-dependent, synchronic and synergistic mechanisms of alcohol-induced cardiac damage. Ethanol alters membrane permeability and composition, interferes with receptors and intracellular transients, induces oxidative, metabolic and energy damage, decreases protein synthesis, excitation-contraction coupling and increases cell apoptosis. In addition, ethanol decreases myocyte protective and repair mechanisms and their regeneration. Although there are diverse different strategies to directly target alcohol-induced heart damage, they are partially effective, and can only be used as support medication in a multidisciplinary approach. Alcohol abstinence is the preferred goal, but control drinking is useful in alcohol-addicted subjects not able to abstain. Correction of nutrition, ionic and vitamin deficiencies and control of alcohol-related systemic organ damage are compulsory. Recently, several growth factors (myostatin, IGF-1, leptin, ghrelin, miRNA, and ROCK inhibitors) and new cardiomyokines such as FGF21 have been described to regulate cardiac plasticity and decrease cardiac damage, improving cardiac repair mechanisms, and they are promising agents in this field. New potential therapeutic targets aim to control oxidative damage, myocyte hypertrophy, interstitial fibrosis and persistent apoptosis In addition, stem-cell therapy may improve myocyte regeneration. However, these strategies are not yet approved for clinical use. View Full-Text
Keywords: alcoholic cardiomyopathy; apoptosis; fibrosis; hypertrophy; regeneration; cardiomyokines; myostatin; IGF-1; FGF21; miRNA alcoholic cardiomyopathy; apoptosis; fibrosis; hypertrophy; regeneration; cardiomyokines; myostatin; IGF-1; FGF21; miRNA

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Fernández-Solà, J.; Planavila Porta, A. New Treatment Strategies for Alcohol-Induced Heart Damage. Int. J. Mol. Sci. 2016, 17, 1651.

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