{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["23(12)"],"submitter":["Canale P"],"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<sub>2</sub>O<sub>2</sub>. Either in the in vivo or in vitro models, T3 administr"],"journal":["International journal of molecular sciences"],"pagination":["6549"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9223604"],"repository":["biostudies-literature"],"pubmed_title":["Role of miR-133/Dio3 Axis in the T3-Dependent Modulation of Cardiac mitoK-ATP Expression."],"pmcid":["PMC9223604"],"pubmed_authors":["Canale P","Nicolini G","Balzan S","Iervasi G","Forini F","Rizzo M","Pitto L","Kusmic C"],"additional_accession":[]},"is_claimable":false,"name":"Role of miR-133/Dio3 Axis in the T3-Dependent Modulation of Cardiac mitoK-ATP Expression.","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<sub>2</sub>O<sub>2</sub>. Either in the in vivo or in vitro models, T3 administr","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2025-04-04T08:48:18.502Z","creation":"2025-04-04T08:48:18.502Z"},"accession":"S-EPMC9223604","cross_references":{"pubmed":["35742991"],"doi":["10.3390/ijms23126549"]}}