MicroRNA and Non-alcoholic fatty liver disease.

Abstract

Nowadays, non-alcoholic fatty liver disease (NAFLD) has become a worldwide health concerned because its prevalence is rising and it is closely associated with metabolic syndrome and cardiovascular disease. NAFLD can be divided into two groups: non-alcoholic fatty liver (steatosis) and non-alcoholic steatohepatitis (NASH). In particular, NASH increases the risk of death compared with general population, and can progress to cirrhosis and hepatocellular carcinoma. MicroRNAs (miR) have been discovered as the crucial in regulating both mRNA and protein expressions which involve diverse physiological and pathological processes such as cell proliferation, inflammation and apoptosis. Numerous microRNAs have been contributed to the pathogenesis of many liver diseases, especially NAFLD. Several studies present that miR-122 plays the major role in hepatic lipid metabolism. Antagomirs of miR-122 are expected to novel treatment strategy for lowering circulating cholesterol but the data are still controversial. Additionally, miR-33 is crucial in cholesterol and fatty acid homeostasis. Interestingly, miR-34a is emerging microRNA for explaining inflammatory process in NAFLD via miR-34a/SIRT1/p53/apoptosis pathway and plays as the regulator of HMGCoA reductase. These pathological mechanisms can be confirmed by studies in both animals and human models. Liver fibrosis is regulated by microRNAs that affect several mechanisms such as hepatic stellate cell activation. For clinical applications, serum microRNAs are studied and developed for noninvasive tool or biomarker for evaluating liver inflammation and fibrosis. MicroRNA-based therapeutics may be the new hope for NAFLD treatment in the future.