ArticleBiochimica et biophysica acta2015
Post-transcriptional regulation of cardiac sodium channel gene SCN5A expression and function by miR-192-5p.
Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.
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Who cites it
32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.
- MicroRNA expression signatures of atrial fibrillation: The critical systematic review and bioinformatics analysis.Experimental biology and medicine (Maywood, N.J.) · 2020Pooled it
- MicroRNAs in Atrial Fibrillation: from Expression Signatures to Functional Implications.Cardiovascular drugs and therapy · 2017Pooled it
- Short SCN5A Transcript Yields a NaV1.5 Fragment Influencing Cardiac Metabolism.Circulation research · 2026Article
- Epigenetic regulation of electromechanical continuity might determine phenotypic heterogeneity in SCN5A mutation carriers in Brugada syndrome.Scientific reports · 2025Article
- Repositioning of antiarrhythmics for prostate cancer treatment: a novel strategy to reprogram cancer-associated fibroblasts towards a tumor-suppressive phenotype.Journal of experimental & clinical cancer research : CR · 2024Article
- Review
- Serum-Circulating microRNAs in Sporadic Inclusion Body Myositis.International journal of molecular sciences · 2023Article
- Multilayer control of cardiac electrophysiology by microRNAs.Journal of molecular and cellular cardiology · 2022Review
- Absolute Quantification of Nav1.5 Expression by Targeted Mass Spectrometry.International journal of molecular sciences · 2022Article
- Genomic and Non-Genomic Regulatory Mechanisms of the Cardiac Sodium Channel in Cardiac Arrhythmias.International journal of molecular sciences · 2022Review
- A narrative review of non-coding RNAs in atrial fibrillation: potential therapeutic targets and molecular mechanisms.Annals of translational medicine · 2021Review
- Re-evaluation of single nucleotide variants and identification of structural variants in a cohort of 45 sudden unexplained death cases.International journal of legal medicine · 2021Article
- Molecular basis of ventricular arrhythmogenicity in a Pgc-1α deficient murine model.Molecular genetics and metabolism reports · 2021Article
- Article
- Genetic Characteristics and Transcriptional Regulation of Sodium Channel Related Genes in Chinese Patients With Brugada Syndrome.Frontiers in cardiovascular medicine · 2021Article
- Emerging Role of MiR-192-5p in Human Diseases.Frontiers in pharmacology · 2021Review
- MIR448 antagomir reduces arrhythmic risk after myocardial infarction by upregulating the cardiac sodium channel.JCI insight · 2020Article
- Genetics and Epigenetics of Atrial Fibrillation.International journal of molecular sciences · 2020Review
- Life Cycle of the Cardiac Voltage-Gated Sodium Channel NaFrontiers in physiology · 2020Review
- A small-molecule LF3 abrogates β-catenin/TCF4-mediated suppression of NaJournal of molecular and cellular cardiology · 2019Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
The SCN5A gene encodes cardiac sodium channel Nav1.5 and causes lethal ventricular arrhythmias/sudden death and atrial fibrillation (AF) when mutated. MicroRNAs (miRNAs) are important post-transcriptional regulators of gene expression, and involved in the pathogenesis of many diseases. However, little is known about the regulation of SCN5A by miRNAs. Here we reveal a novel post-transcriptional regulatory mechanism for expression and function of SCN5A/Nav1.5 via miR-192-5p. Bioinformatic analysis revealed that the 3'-UTR of human and rhesus SCN5A, but not elephant, pig, rabbit, mouse, and rat SCN5A, contained a target binding site for miR-192-5p and dual luciferase reporter assays showed that the site was critical for down-regulation of human SCN5A. With Western blot assays and electrophysiological studies, we demonstrated that miR-192-5p significantly reduced expression of SCN5A and Nav1.5 as well as peak sodium current density INa generated by Nav1.5. Notably, in situ hybridization, immunohistochemistry and real-time qPCR analyses showed that miR-192-5p was up-regulated in tissue samples from AF patients, which was associated with down-regulation of SCN5A/Nav1.5. These results demonstrate an important post-transcriptional role of miR-192-5p in post-transcriptional regulation of Nav1.5, reveal a novel role of miR-192-5p in cardiac physiology and disease, and provide a new target for novel miRNA-based antiarrhythmic therapy for diseases with reduced INa.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.