Alcohol consumption prompts detrimental psychological, pathophysiological and health issues, representing one of the major causes of death worldwide. Alcohol use disorder (AUD), which is characterized by compulsive alcohol intake and loss of control over alcohol usage, arises from a complex interplay between genetic and environmental factors. More importantly, long-term abuse of alcohol is often tied with unfavorable cardiac remodeling and contractile alterations, a cadre of cardiac responses collectively known as alcoholic cardiomyopathy (ACM). Recent evidence has denoted a pivotal role for ethanol-triggered epigenetic modifications, the interface between genome and environmental cues, in the organismal and cellular responses to ethanol exposure. To-date, three major epigenetic mechanisms (DNA methylation, histone modifications, and RNA-based mechanisms) have been identified for the onset and development of AUD and ACM. Importantly, these epigenetic changes induced by alcohol may be detectable in the blood, thus offering diagnostic, therapeutic, and prognostic promises of epigenetic markers for AUD and alcoholic complications. In addition, several epigenetic drugs have shown efficacies in the management of alcohol abuse, loss of control for alcohol usage, relapse, drinking-related anxiety and behavior in withdrawal. In this context, medications targeting epigenetic modifications may hold promises for pharmaceutical management of AUD and ACM.
Keywords: Alcohol use disorder; Alcoholic cardiomyopathy; DNA methylation; DNMT inhibitor; Epigenetics; HDAC inhibitor; Histone modification; Non-coding RNA.
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