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• W3193559194 endingPage "112787" @default.
• W3193559194 startingPage "112787" @default.
• W3193559194 abstract "Non-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." @default.
• W3193559194 created "2021-08-30" @default.
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• W3193559194 date "2021-10-01" @default.
• W3193559194 modified "2023-10-09" @default.
• W3193559194 title "miR-23b Ameliorates nonalcoholic steatohepatitis by targeting Acyl-CoA thioesterases 4" @default.
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• W3193559194 doi "https://doi.org/10.1016/j.yexcr.2021.112787" @default.
• W3193559194 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34450119" @default.
• W3193559194 hasPublicationYear "2021" @default.
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