{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sun H"],"funding":["Foundation for the National Institutes of Health","University of Minnesota","National Institutes of Health"],"pagination":["101603"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9515436"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["66"],"pubmed_abstract":["<h4>Objective</h4>Obesity-associated nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver failure and death. However, the pathogenesis of NAFLD and its severe form, nonalcoholic steatohepatitis (NASH), is poorly understood. The energy sensor, AMP-activated protein kinase (AMPK), has decreased activity in obesity and NAFLD, but the mechanisms are unclear. Here, we examined whether obesity-induced miR-802 has a role in promoting NASH by targeting AMPK. We also investigated whether miR-802 and AMPK have roles in modulating beneficial therapeutic effects mediated by obeticholic acid (OCA), a promising clinical agent for NASH.<h4>Methods</h4>Immunoblotting, luciferase assays, and RNA-protein interaction studies were performed to test whether miR-802 directly targets AMPK. The ro"],"journal":["Molecular metabolism"],"pubmed_title":["Obesity-induced miR-802 directly targets AMPK and promotes nonalcoholic steatohepatitis in mice."],"pmcid":["PMC9515436"],"funding_grant_id":["HHSN276201200017C","DK095842","DK062777"],"pubmed_authors":["Seok S","Jung H","Kemper B","Kemper JK","Sun H"],"additional_accession":[]},"is_claimable":false,"name":"Obesity-induced miR-802 directly targets AMPK and promotes nonalcoholic steatohepatitis in mice.","description":"<h4>Objective</h4>Obesity-associated nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver failure and death. However, the pathogenesis of NAFLD and its severe form, nonalcoholic steatohepatitis (NASH), is poorly understood. The energy sensor, AMP-activated protein kinase (AMPK), has decreased activity in obesity and NAFLD, but the mechanisms are unclear. Here, we examined whether obesity-induced miR-802 has a role in promoting NASH by targeting AMPK. We also investigated whether miR-802 and AMPK have roles in modulating beneficial therapeutic effects mediated by obeticholic acid (OCA), a promising clinical agent for NASH.<h4>Methods</h4>Immunoblotting, luciferase assays, and RNA-protein interaction studies were performed to test whether miR-802 directly targets AMPK. The ro","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2025-04-22T06:19:52.534Z","creation":"2025-04-05T21:42:55.9Z"},"accession":"S-EPMC9515436","cross_references":{"pubmed":["36126896"],"doi":["10.1016/j.molmet.2022.101603"]}}