<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(10)</volume><submitter>Forini F</submitter><pubmed_abstract>The LncRNA my-heart (Mhrt) and the chromatin remodeler Brg1 inhibit each other to respectively prevent or favor the maladaptive α-myosin-heavy-chain (Myh6) to β-myosin-heavy-chain (Myh7) switch, so their balance crucially guides the outcome of cardiac remodeling under stress conditions. Even though triiodothyronine (T3) has long been recognized as a critical regulator of the cardiac Myh isoform composition, its role as a modulator of the Mhrt/Brg1 axis is still unexplored. Here the effect of T3 on the Mhrt/Brg1 regulatory circuit has been analyzed in relation with chromatin remodeling and previously identified T3-dependent miRNAs. The expression levels of Mhrt, Brg1 and Myh6/Myh7 have been assessed in rat models of hyperthyroidism or acute myocardial ischemia/reperfusion (IR) treated with </pubmed_abstract><journal>Cells</journal><pagination>E2155</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7598656</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>T3 Critically Affects the Mhrt/Brg1 Axis to Regulate the Cardiac MHC Switch: Role of an Epigenetic Cross-Talk.</pubmed_title><pmcid>PMC7598656</pmcid><pubmed_authors>D'Aurizio R</pubmed_authors><pubmed_authors>Nicolini G</pubmed_authors><pubmed_authors>Iervasi G</pubmed_authors><pubmed_authors>Forini F</pubmed_authors><pubmed_authors>Pitto L</pubmed_authors><pubmed_authors>Mercatanti A</pubmed_authors><pubmed_authors>Kusmic C</pubmed_authors></additional><is_claimable>false</is_claimable><name>T3 Critically Affects the Mhrt/Brg1 Axis to Regulate the Cardiac MHC Switch: Role of an Epigenetic Cross-Talk.</name><description>The LncRNA my-heart (Mhrt) and the chromatin remodeler Brg1 inhibit each other to respectively prevent or favor the maladaptive α-myosin-heavy-chain (Myh6) to β-myosin-heavy-chain (Myh7) switch, so their balance crucially guides the outcome of cardiac remodeling under stress conditions. Even though triiodothyronine (T3) has long been recognized as a critical regulator of the cardiac Myh isoform composition, its role as a modulator of the Mhrt/Brg1 axis is still unexplored. Here the effect of T3 on the Mhrt/Brg1 regulatory circuit has been analyzed in relation with chromatin remodeling and previously identified T3-dependent miRNAs. The expression levels of Mhrt, Brg1 and Myh6/Myh7 have been assessed in rat models of hyperthyroidism or acute myocardial ischemia/reperfusion (IR) treated with </description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Sep</publication><modification>2026-05-01T01:25:45.013Z</modification><creation>2020-11-03T08:03:16Z</creation></dates><accession>S-EPMC7598656</accession><cross_references><pubmed>32987653</pubmed><doi>10.3390/cells9102155</doi></cross_references></HashMap>