ArticlePloS one2014
MiRNA-1/133a clusters regulate adrenergic control of cardiac repolarization.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Genetic and epigenetic landscape of non-familial sudden cardiac death.Molecular biology reports · 2026Review
- MRGBMDAT: a multi-relational graph encoder network with bilinear fusion for miRNA-disease association type prediction.Bioinformatics (Oxford, England) · 2026Article
- Trdn-as directs m6A-dependent transcriptional termination for accurate triadin isoform switching, preventing aberrant dyads and cardiomyopathy.Nature communications · 2026Article
- Are RNA Therapies a Solid Foundation or a Frontier Yet to Be Conquered?International journal of molecular sciences · 2026Review
- Exosomal mir-126-3p derived from endothelial cells induces ion channel dysfunction by targeting RGS3 signaling in cardiomyocytes: a novel mechanism in Takotsubo cardiomyopathy.Stem cell research & therapy · 2025Article
- MicroRNAs in atrial fibrillation - have we discovered the Holy Grail or opened a Pandora's box?Frontiers in pharmacology · 2025Review
- Regional random mutagenesis driven by multiple sgRNAs and diverse on-target genome editing events to identify functionally important elements in non-coding regions.Open biology · 2024Article
- Non-Coding RNA-Targeted Therapy: A State-of-the-Art Review.International journal of molecular sciences · 2024Review
- The Roles of microRNAs in the Cardiovascular System.International journal of molecular sciences · 2023Review
- Control of CRK-RAC1 activity by the miR-1/206/133 miRNA family is essential for neuromuscular junction function.Nature communications · 2022Article
- MicroRNAs as therapeutic targets in cardiovascular disease.The Journal of clinical investigation · 2022Review
- Repression ofScience advances · 2021Article
- Article
- Circulating microRNAs fluctuations in exercise-induced cardiac remodeling: A systematic review.American journal of translational research · 2021Review
- Cardiac dopamine D1 receptor triggers ventricular arrhythmia in chronic heart failure.Nature communications · 2020Article
- MiR-1/133 attenuates cardiomyocyte apoptosis and electrical remodeling in mice with viral myocarditis.Cardiology journal · 2020Article
- Ubiquitin‑proteasomes are the dominant mediators of the regulatory effect of microRNA‑1 on cardiac remodeling after myocardial infarction.International journal of molecular medicine · 2019Article
- miR-1, miR-499 and miR-208 are sensitive markers to diagnose sudden death due to early acute myocardial infarction.Journal of cellular and molecular medicine · 2019Article
- MicroRNAs in Cardiac Diseases.Cells · 2019Review
- The Three Paralogous MicroRNA Clusters in Development and Disease, miR-17-92, miR-106a-363, and miR-106b-25.Scientifica · 2016Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The electrical properties of the heart are primarily determined by the activity of ion channels and the activity of these molecules is permanently modulated and adjusted to the physiological needs by adrenergic signaling. miRNAs are known to control the expression of many proteins and to fulfill distinct functions in the mammalian heart, though the in vivo effects of miRNAs on the electrical activity of the heart are poorly characterized. The miRNAs miR-1 and miR-133a are the most abundant miRNAs of the heart and are expressed from two miR-1/133a genomic clusters. Genetic modulation of miR-1/133a cluster expression without concomitant severe disturbance of general cardiomyocyte physiology revealed that these miRNA clusters govern cardiac muscle repolarization. Reduction of miR-1/133a dosage induced a longQT phenotype in mice especially at low heart rates. Longer action potentials in cardiomyocytes are caused by modulation of the impact of β-adrenergic signaling on the activity of the depolarizing L-type calcium channel. Pharmacological intervention to attenuate β-adrenergic signaling or L-type calcium channel activity in vivo abrogated the longQT phenotype that is caused by modulation of miR-1/133a activity. Thus, we identify the miR-1/133a miRNA clusters to be important to prevent a longQT-phenotype in the mammalian heart.
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