ArticleJournal of the American Heart Association2016
Contrasting Nav1.8 Activity in Scn10a-/- Ventricular Myocytes and the Intact Heart.
Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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
21 citing papers in PubMed, 26 citations in OpenAlex.
- MOG1medRxiv : the preprint server for health sciences · 2025Article
- Voltage-gated sodium channels in excitable cells as drug targets.Nature reviews. Drug discovery · 2025Review
- 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
- Mechanisms of torsades de pointes: an update.Frontiers in cardiovascular medicine · 2024Review
- Brugada Syndrome: From Molecular Mechanisms and Genetics to Risk Stratification.International journal of molecular sciences · 2023Review
- Late Sodium Current of the Heart: Where Do We Stand and Where Are We Going?Pharmaceuticals (Basel, Switzerland) · 2022Review
- Rotors anchored by refractory islands drive torsades de pointes in an experimental model of electrical storm.Heart rhythm · 2022Article
- Common variants in SCN10A gene associated with Brugada syndrome.Human molecular genetics · 2021Article
- Ranolazine: An Old Drug with Emerging Potential; Lessons from Pre-Clinical and Clinical Investigations for Possible Repositioning.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Detrimental proarrhythmogenic interaction of CaNature communications · 2021Article
- Role of Non-Coding Variants in Brugada Syndrome.International journal of molecular sciences · 2020Review
- From Genome-Wide Association Studies to Cardiac Electrophysiology: Through the Maze of Biological Complexity.Frontiers in physiology · 2020Review
- The Role of Voltage-Gated Sodium Channel 1.8 in the Effect of Atropine on Heart Rate: Evidence From a Retrospective Clinical Study and Mouse Model.Frontiers in pharmacology · 2020Article
- Absence of Functional NaCardiovascular drugs and therapy · 2019Article
- Functional characterization of SCN10A variants in several cases of sudden unexplained death.Forensic science international · 2019Article
- A Distinct Pool of NaFrontiers in physiology · 2019Article
- Transcriptomic analyses of murine ventricular cardiomyocytes.Scientific data · 2018Article
- Common Coding Variants inCirculation. Genomic and precision medicine · 2018Article
- Deleterious protein-altering mutations in the SCN10A voltage-gated sodium channel gene are associated with prolonged QT.Clinical genetics · 2018Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGenome-wide association studies have implicated variants in SCN10A, which encodes Nav1.8, as modulators of cardiac conduction. Follow-up work has indicated the SCN10A sequence includes an intronic enhancer for SCN5A. Yet the role of the Nav1.8 protein in the myocardium itself is still unclear. To investigate this, we use homozygous knockout mice (Scn10a METHODS AND
resultsWe previously reported that pharmacologic blockade of Nav1.8 in wild-type animals blunts action potential prolongation by ATX-II at slow drive rates (≤1 Hz). Here we present evidence of the same blunting in Scn10a
conclusionsWhile Scn10a transcripts are not detectible in ventricular cardiomyocytes, gene deletion results in reproducible loss of late sodium current under extreme experimental conditions. However, there are no identifiable consequences of this Scn10a deletion in the intact mouse heart at usual rates. These findings argue that common variants in SCN10A that affect ventricular conduction do so by modulating SCN5A.
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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.