Liver fibrosis is a complex pathological process caused by multiple pathogenic factors，such as ethanol, viruses, toxins, drugs or cholestasis, and it can eventually develop into liver cirrhosis without effective treatment. Activation of hepatic stellate cells (HSCs) is a pivotal cellular event in the pathogenesis of liver fibrosis. However, the pathogenesis of liver fibrosis has not been fully elucidated. DNA/RNA methylation can regulate gene expression without alteration in its sequence, and numerous studies have shown the involvement of DNA methylation in the activation of HSCs and then promote the progression of liver fibrosis. In addition, RNA methylation has recently been reported to play a regulatory role in this process. In this review, we focus on the aberrant DNA/RNA methylation of selected genes and explore their functional mechanism in regulating HSCs activation and liver fibrogenesis. All of these findings will enhance our understanding of DNA/RNA methylation and their roles in liver fibrosis and provide the basis to identify effective therapeutic targets.
Keywords: DNMTs; Hepatic stellate cells (HSCs); Liver fibrosis; Methylation; m(6)A.
Copyright © 2021. Published by Elsevier Inc.