<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>23(12)</volume><submitter>Canale P</submitter><pubmed_abstract>The opening of the ATP-sensitive mitochondrial potassium channel (mitok-ATP) is a common goal of cardioprotective strategies in the setting of acute and chronic myocardial disease. The biologically active thyroid hormone (TH), 3-5-3-triiodothyronine (T3), has been indicated as a potential activator of mitoK-ATP but the underlying mechanisms are still elusive. Here we describe a novel role of T3 in the transcriptional regulation of mitoK and mitoSur, the recently identified molecular constituents of the channel. To mimic human ischemic heart damage, we used a rat model of a low T3 state as the outcome of a myocardial ischemia/reperfusion event, and neonatal rat cardiomyocytes (NRCM) challenged with hypoxia or H&lt;sub>2&lt;/sub>O&lt;sub>2&lt;/sub>. Either in the in vivo or in vitro models, T3 administr</pubmed_abstract><journal>International journal of molecular sciences</journal><pagination>6549</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9223604</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Role of miR-133/Dio3 Axis in the T3-Dependent Modulation of Cardiac mitoK-ATP Expression.</pubmed_title><pmcid>PMC9223604</pmcid><pubmed_authors>Canale P</pubmed_authors><pubmed_authors>Nicolini G</pubmed_authors><pubmed_authors>Balzan S</pubmed_authors><pubmed_authors>Iervasi G</pubmed_authors><pubmed_authors>Forini F</pubmed_authors><pubmed_authors>Rizzo M</pubmed_authors><pubmed_authors>Pitto L</pubmed_authors><pubmed_authors>Kusmic C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Role of miR-133/Dio3 Axis in the T3-Dependent Modulation of Cardiac mitoK-ATP Expression.</name><description>The opening of the ATP-sensitive mitochondrial potassium channel (mitok-ATP) is a common goal of cardioprotective strategies in the setting of acute and chronic myocardial disease. The biologically active thyroid hormone (TH), 3-5-3-triiodothyronine (T3), has been indicated as a potential activator of mitoK-ATP but the underlying mechanisms are still elusive. Here we describe a novel role of T3 in the transcriptional regulation of mitoK and mitoSur, the recently identified molecular constituents of the channel. To mimic human ischemic heart damage, we used a rat model of a low T3 state as the outcome of a myocardial ischemia/reperfusion event, and neonatal rat cardiomyocytes (NRCM) challenged with hypoxia or H&lt;sub>2&lt;/sub>O&lt;sub>2&lt;/sub>. Either in the in vivo or in vitro models, T3 administr</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2025-04-04T08:48:18.502Z</modification><creation>2025-04-04T08:48:18.502Z</creation></dates><accession>S-EPMC9223604</accession><cross_references><pubmed>35742991</pubmed><doi>10.3390/ijms23126549</doi></cross_references></HashMap>