<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sun H</submitter><funding>Foundation for the National Institutes of Health</funding><funding>University of Minnesota</funding><funding>National Institutes of Health</funding><pagination>101603</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9515436</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>66</volume><pubmed_abstract>&lt;h4>Objective&lt;/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.&lt;h4>Methods&lt;/h4>Immunoblotting, luciferase assays, and RNA-protein interaction studies were performed to test whether miR-802 directly targets AMPK. The ro</pubmed_abstract><journal>Molecular metabolism</journal><pubmed_title>Obesity-induced miR-802 directly targets AMPK and promotes nonalcoholic steatohepatitis in mice.</pubmed_title><pmcid>PMC9515436</pmcid><funding_grant_id>HHSN276201200017C</funding_grant_id><funding_grant_id>DK095842</funding_grant_id><funding_grant_id>DK062777</funding_grant_id><pubmed_authors>Seok S</pubmed_authors><pubmed_authors>Jung H</pubmed_authors><pubmed_authors>Kemper B</pubmed_authors><pubmed_authors>Kemper JK</pubmed_authors><pubmed_authors>Sun H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Obesity-induced miR-802 directly targets AMPK and promotes nonalcoholic steatohepatitis in mice.</name><description>&lt;h4>Objective&lt;/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.&lt;h4>Methods&lt;/h4>Immunoblotting, luciferase assays, and RNA-protein interaction studies were performed to test whether miR-802 directly targets AMPK. The ro</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Sep</publication><modification>2025-04-22T06:19:52.534Z</modification><creation>2025-04-05T21:42:55.9Z</creation></dates><accession>S-EPMC9515436</accession><cross_references><pubmed>36126896</pubmed><doi>10.1016/j.molmet.2022.101603</doi></cross_references></HashMap>