ArticleCirculation research2012
Blocking Scn10a channels in heart reduces late sodium current and is antiarrhythmic.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
104 citing papers in PubMed, 2 syntheses or guidelines pooled it, 165 citations in OpenAlex.
- Genetic Determinants of Electrocardiographic P-Wave Duration and Relation to Atrial Fibrillation.Circulation. Genomic and precision medicine · 2020Pooled it
- Common and Rare Coding Genetic Variation Underlying the Electrocardiographic PR Interval.Circulation. Genomic and precision medicine · 2018Pooled it
- Common and rare variants in SCN10A modulate the risk of atrial fibrillation.Circulation. Cardiovascular genetics · 2015Trial
- Genome- and phenome-wide analyses of cardiac conduction identifies markers of arrhythmia risk.Circulation · 2013Trial
- Targeting Arrhythmogenic Late Sodium Current by FHF1Circulation research · 2026Article
- MOG1medRxiv : the preprint server for health sciences · 2025Article
- Ventricular ion channels and arrhythmias: an overview of physiology, pathophysiology and pharmacology.Medical review (2021) · 2025Review
- Voltage-gated sodium channels in excitable cells as drug targets.Nature reviews. Drug discovery · 2025Review
- Atrial APD prolongation caused by the upregulation of RAGE and subsequentActa biochimica et biophysica Sinica · 2025Article
- Review
- Characterization of novel arrhythmogenic patterns arising secondary to heterogeneous expression and activation of Nav1.8.Frontiers in cardiovascular medicine · 2025Article
- NaInternational journal of molecular sciences · 2024Article
- Using Omics to Identify Novel Therapeutic Targets in Heart Failure.Circulation. Genomic and precision medicine · 2024Review
- Mechanisms of torsades de pointes: an update.Frontiers in cardiovascular medicine · 2024Review
- Patient-specific induced pluripotent stem cell properties implicate CaPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
- A novel co-target of ACY1 governing plasma membrane translocation of SphK1 contributes to inflammatory and neuropathic pain.iScience · 2023Article
- Molecular and Functional Relevance of NaInternational journal of molecular sciences · 2023Article
- Brugada Syndrome: From Molecular Mechanisms and Genetics to Risk Stratification.International journal of molecular sciences · 2023Review
- Structural basis for high-voltage activation and subtype-specific inhibition of human NaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Delayed Ventricular Repolarization and Sodium Channel Current Modification in a Mouse Model of Rett Syndrome.International journal of molecular sciences · 2022Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
rationaleAlthough the sodium channel locus SCN10A has been implicated by genome-wide association studies as a modulator of cardiac electrophysiology, the role of its gene product Nav1.8 as a modulator of cardiac ion currents is unknown.
objectiveWe determined the electrophysiological and pharmacological properties of Nav1.8 in heterologous cell systems and assessed the antiarrhythmic effect of Nav1.8 block on isolated mouse and rabbit ventricular cardiomyocytes. METHODS AND
resultsWe first demonstrated that Scn10a transcripts are identified in mouse heart and that the blocker A-803467 is highly specific for Nav1.8 current over that of Nav1.5, the canonical cardiac sodium channel encoded by SCN5A. We then showed that low concentrations of A-803467 selectively block "late" sodium current and shorten action potentials in mouse and rabbit cardiomyocytes. Exaggerated late sodium current is known to mediate arrhythmogenic early afterdepolarizations in heart, and these were similarly suppressed by low concentrations of A-803467.
conclusionsScn10a expression contributes to late sodium current in heart and represents a new target for antiarrhythmic intervention.
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What OpenQuestion holds
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.