ReviewNature reviews. Cardiology2009
Sodium channel mutations and arrhythmias.
Review in Nature reviews. Cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
143 citing papers in PubMed, 311 citations in OpenAlex.
- The History of the Precordial Early Repolarization and Sudden Death Syndrome, Lately Named Brugada Syndrome.Journal of clinical medicine · 2026Review
- PersonalizedFrontiers in physiology · 2026Article
- The differential impacts of equivalent gating-charge mutations in voltage-gated sodium channels.The Journal of general physiology · 2025Article
- Exploring epicardial arrhythmogenic substrates in long QT syndrome type III overlapping with J-wave syndrome.HeartRhythm case reports · 2025Article
- Cardiac Conduction Delay for Sodium Channel Antagonist Antiseizure Medications: An Analysis of the Canadian Longitudinal Study on Aging.Neurology · 2025Article
- Binding ofeLife · 2025Article
- Cellular interactions and Ion channel signatures in atrial fibrillation remodeling: insights from single-cell analysis and machine learning.Frontiers in cardiovascular medicine · 2025Article
- Integrated proteomics and transcriptomics analysis reveals insights into differences in premature mortality associated with disparate pathogenic RBM20 variants.Journal of molecular and cellular cardiology · 2024Article
- NaV1.5 autoantibodies in Brugada syndrome: pathogenetic implications.European heart journal · 2024Article
- Mapping structural distribution and gating-property impacts of disease-associated mutations in voltage-gated sodium channels.iScience · 2024Article
- ELUCIDATING THE DIFFERENTIAL IMPACTS OF EQUIVALENT GATING-CHARGE MUTATIONS IN VOLTAGE-GATED SODIUM CHANNELS.bioRxiv : the preprint server for biology · 2024Article
- Article
- Proof of concept for monoclonal antibody therapy in a cellular model of acquired long QT syndrome type 3.American journal of physiology. Heart and circulatory physiology · 2024Article
- The Extent of Edgetic Perturbations in the Human Interactome Caused by Population-Specific Mutations.Biomolecules · 2023Article
- Bacterial sodium channels as gene therapy for cardiac arrhythmia: slow (activation and inactivation kinetics) and steady wins the race.American journal of physiology. Heart and circulatory physiology · 2023Article
- Differential regulation of cardiac sodium channels by intracellular fibroblast growth factors.The Journal of general physiology · 2023Article
- NaV1.6 dysregulation within myocardial T-tubules by D96V calmodulin enhances proarrhythmic sodium and calcium mishandling.The Journal of clinical investigation · 2023Article
- Emerging methods to model cardiac ion channel and myocyte electrophysiology.Biophysics reviews · 2023Review
- The Exciting Realities and Possibilities of iPS-Derived Cardiomyocytes.Bioengineering (Basel, Switzerland) · 2023Review
- Case Report:Frontiers in cardiovascular medicine · 2023Article
83 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since the identification of the first SCN5A mutation associated with long QT syndrome in 1995, several mutations in this gene for the alpha subunit of the cardiac sodium channel have been identified in a heterogeneous subset of cardiac rhythm syndromes, including Brugada syndrome, progressive cardiac conduction defect, sick sinus node syndrome, atrial fibrillation and dilated cardiomyopathy. Robust clinical evidence has been accompanied by bench studies performed in different models spanning from in vitro expression systems to transgenic mice. Together, these studies have helped establish genotype-phenotype correlations and have shaped our understanding of the role of the cardiac sodium channel in health and in disease. Remarkably, these advances in understanding have impacted on clinical management by allowing us to start developing gene-specific risk stratification schemes and mutation-specific management strategies. In this Review, we summarize the current understanding of the molecular mechanism of SCN5A-associated inherited arrhythmias, focusing on the most recent development of mutation-specific management in SCN5A-associated long QT syndrome type 3. We also briefly discuss arrhythmia-causing mutations in the genes encoding the beta subunit of the cardiac sodium channel and in those encoding proteins in the associated macromolecular complex.
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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.