Epigenetic modification in alcohol-related liver diseases

Alcohol-related liver disease (ARLD) refers to a spectrum of hepatic damage triggered by excessive alcohol intake, resulting in inflamed and swollen livers, ultimately, liver cirrhosis. Alcoholic liver disease (ALD) is a similar term denoting liver disorders encompassing steatosis, cirrhosis, and hepatocellular carcinoma. Recent evidence has suggested a vital role for epigenetic factors, which modulate gene expression in the absence of changes in DNA sequence, in the onset and progression of liver disorders, to foster hepatic fibrogenesis and cirrhosis. Mounting findings have delineated that alcohol consumption extensively modulates liver epigenetics, thus, prompting the etiology of ARLD and ALD. Alcohol-induced epigenetic modifications (AIEM) in the liver encompass histone modification, microRNA-induced genetic modulation, DNA methylation, and alcohol-evoked cell signaling that alters gene expression. Herein, we aim at summarizing key findings to decipher AIEM and its role in the onset and development of ARLD and ALD from the perspectives of both cellular and animal models of alcohol exposure. Furthermore, we will share our viewpoints on epigenetics-based therapeutic options in the management of ARLD and ALD.