[Histone deacetylases and alcohol-related liver disease]

Alcohol-related liver disease (ALD) is a common chronic liver disease caused by prolonged excessive alcohol consumption. It may initially be asymptomatic or manifest as mild alcoholic fatty liver, then progress to subclinical steatohepatitis characterized by hepatic inflammation, and eventually develop into fibrosis, cirrhosis, liver failure, or even hepatocellular carcinoma. Although alcohol abstinence remains the primary strategy for ALD management, its effectiveness is often limited by patient adherence and social factors, making combined pharmacological intervention necessary in many cases. Histone deacetylase (HDAC), which is a key enzyme involved in post-translational protein modification, have been implicated in the pathogenesis and progression of ALD through their regulation of lipid metabolism, inflammatory responses, and fibrosis, and are therefore considered promising therapeutic targets. Various HDAC-related agonists and inhibitors have shown therapeutic potential in ALD, but their subtype-specific roles and clinical relevance remain to be fully elucidated. This review systematically summarizes the roles of HDAC and their agonists or inhibitors in ALD, in order to provide insight into the mechanisms of ALD progression and to support the development of precise therapeutic strategies and clinical translation.