miR-23b Ameliorates Nonalcoholic Steatohepatitis by Targeting Acyl-CoA thioesterases 4

Exp Cell Res. 2021 Aug 24:112787. doi: 10.1016/j.yexcr.2021.112787. Online ahead of print.ABSTRACTNon-alcoholic fatty liver disease (NAFLD) and its more advanced stages, Non-alcoholic steatohepatitis and Cirrhosis, are the most common liver diseases in the worldwide, especially in developing countries. NAFLD is distinguished by the accumulation of triglycerides within hepatocytes. An increasing body of evidence suggests that hepatic MicroRNAs play an important role in NAFLD by controlling lipid metabolism, inflammation, and fibrosis. However, the precise causative functions of miRNA in NAFLD remain unknown. Here, we discovered that mice lacking MicroRNA-23b developed NAFLD-like phenotypes such as increased serum triglyceride and lipid droplet accumulation. In db/db mice fed a high fat diet, MicroRNA-23b overexpression reduced liver weight and alleviated liver inflammation, apoptosis, and fibrosis. MicroRNA-23b regulates the acyl-CoA metabolic process via Acyl-CoA thioesterase 4 (Acot4), which interacts with Acetyl CoA Carboxylase (ACC), according to the RNA-seq analysis.PMID:34450119 | DOI:10.1016/j.yexcr.2021.112787

Source: Experimental Cell Research - August 27, 2021 Category: Cytology Authors: Hongzhi Li Xiang Li Shanshan Yu Yanling Hu Licheng Xu Tianhe Wang Xiaohong Yang Xinyi Sun Binghai Zhao Source Type: research