ArticleInternational journal of molecular sciences2022
Role of miR-133/Dio3 Axis in the T3-Dependent Modulation of Cardiac mitoK-ATP Expression.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Noncoding RNA as potential therapeutics to rescue mitochondrial dysfunction in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2025Pooled it
- [Targeted inhibition of miR-503 upregulates Apelin expression to alleviate myocardial infarction in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Anticoagulation Therapies and microRNAs in Heart Failure.Biomolecules · 2025Review
- Critical analysis of descriptive microRNA data in the translational research on cardioprotection and cardiac repair: lost in the complexity of bioinformatics.Basic research in cardiology · 2025Review
- Engineered model of heart tissue repair for exploring fibrotic processes and therapeutic interventions.Nature communications · 2024Article
- A landscape of mouse mitochondrial small non-coding RNAs.PloS one · 2024Article
- Novel Transcriptomic Interactomes of Noncoding RNAs in the Heart under Altered Thyroid Hormonal States.International journal of molecular sciences · 2023Article
- Editorial for Special Issue: "MicroRNA in Cardiac Health and Disease".International journal of molecular sciences · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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
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