<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cheng X</submitter><funding>NHLBI NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIGMS NIH HHS</funding><pagination>101977</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11267048</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>86</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) continues to rise with the increasing obesity epidemic. Rezdiffra as an activator of a thyroid hormone receptor-beta is the only Food and Drug Administration approved therapy. As such, there is a critical need to improve our understanding of gene expression regulation and signaling transduction in MASLD to develop new therapies. Matrin-3 is a DNA- and RNA-binding protein involved in the pathogenesis of human diseases. Here we examined its previously uncharacterized role in limiting hepatic steatosis and stress response via the constitutive androstane receptor (CAR).&lt;h4>Methods&lt;/h4>Matrin-3 floxed and liver-specific knockout mice were fed either a chow diet or 60 kcal% high-fat diet (HFD) fo</pubmed_abstract><journal>Molecular metabolism</journal><pubmed_title>Liver matrin-3 protects mice against hepatic steatosis and stress response via constitutive androstane receptor.</pubmed_title><pmcid>PMC11267048</pmcid><funding_grant_id>R01 GM147913</funding_grant_id><funding_grant_id>R01 HL150536</funding_grant_id><pubmed_authors>Zhao M</pubmed_authors><pubmed_authors>Riethoven JJ</pubmed_authors><pubmed_authors>Moran M</pubmed_authors><pubmed_authors>Baki VB</pubmed_authors><pubmed_authors>Liu B</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Harris EN</pubmed_authors><pubmed_authors>Gurumurth CB</pubmed_authors><pubmed_authors>Yu J</pubmed_authors><pubmed_authors>Sun X</pubmed_authors><pubmed_authors>Cheng X</pubmed_authors></additional><is_claimable>false</is_claimable><name>Liver matrin-3 protects mice against hepatic steatosis and stress response via constitutive androstane receptor.</name><description>&lt;h4>Objective&lt;/h4>The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) continues to rise with the increasing obesity epidemic. Rezdiffra as an activator of a thyroid hormone receptor-beta is the only Food and Drug Administration approved therapy. As such, there is a critical need to improve our understanding of gene expression regulation and signaling transduction in MASLD to develop new therapies. Matrin-3 is a DNA- and RNA-binding protein involved in the pathogenesis of human diseases. Here we examined its previously uncharacterized role in limiting hepatic steatosis and stress response via the constitutive androstane receptor (CAR).&lt;h4>Methods&lt;/h4>Matrin-3 floxed and liver-specific knockout mice were fed either a chow diet or 60 kcal% high-fat diet (HFD) fo</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Aug</publication><modification>2026-06-01T13:27:19.899Z</modification><creation>2025-04-19T13:10:30.969Z</creation></dates><accession>S-EPMC11267048</accession><cross_references><pubmed>38936659</pubmed><doi>10.1016/j.molmet.2024.101977</doi></cross_references></HashMap>