ReviewCardiovascular research2013
The arrhythmogenic consequences of increasing late INa in the cardiomyocyte.
Review in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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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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
71 citing papers in PubMed, 135 citations in OpenAlex.
- Stress-Induced Down-Regulation of CPEB4 Disrupts Sodium Channel Regulation and Myocardial Excitability.JACC. Basic to translational science · 2026Article
- Conventional Antiarrhythmics Class I-IV, Late INa Inhibitors, IKs Enhancers, RyR2 Stabilizers, Gap Junction Modulators, Atrial-Selective Antiarrhythmics, and Stable Gastric Pentadecapeptide BPC 157 as Useful Cytoprotective Therapy in Arrhythmias.Pharmaceuticals (Basel, Switzerland) · 2026Review
- The impact of the PI3K/AKT pathway on arrhythmia: mechanisms of action and therapeutic potential.Journal of molecular histology · 2026Review
- Article
- Comparison of clinical outcomes between catheter ablation and permanent pacemaker implantation in Tachycardia-Bradycardia Syndrome patients: a meta-analysis.International journal of cardiology. Heart & vasculature · 2025Article
- Voltage-Gated Sodium Channels: A Therapeutic Target in Ischemic Heart Disease.Reviews in cardiovascular medicine · 2025Review
- An Electromechanical Model-Based Study on the Dosage Effects of Ranolazine in Treating Failing HCM Cardiomyocyte.Cellular and molecular bioengineering · 2025Article
- SUMO Regulation of Ion Channels in Health and Disease.Physiology (Bethesda, Md.) · 2025Review
- Long QT syndrome type 3 gain-of-function of NaCommunications biology · 2025Article
- Cardiovascular safety pharmacology: beyond arrhythmic risk assessment.Frontiers in cardiovascular medicine · 2025Review
- Characterization of novel arrhythmogenic patterns arising secondary to heterogeneous expression and activation of Nav1.8.Frontiers in cardiovascular medicine · 2025Article
- Effects of Eleclazine (GS6615) on the proarrhythmic electrophysiological changes induced by myocardial stretch.Frontiers in physiology · 2025Article
- Empagliflozin inhibits increased Na influx in atrial cardiomyocytes of patients with HFpEF.Cardiovascular research · 2024Article
- The inotropic and arrhythmogenic effects of acutely increased late IFrontiers in cardiovascular medicine · 2024Article
- Selective Inhibition of Cardiac Late NaBiomedicines · 2023Article
- Caveolin-3 and Caveolae regulate ventricular repolarization.Journal of molecular and cellular cardiology · 2023Article
- Fibroblast growth factor homologous factors serve as a molecular rheostat in tuning arrhythmogenic cardiac late sodium current.Nature cardiovascular research · 2022Article
- Late Sodium Current of the Heart: Where Do We Stand and Where Are We Going?Pharmaceuticals (Basel, Switzerland) · 2022Review
- Engineered bacterial voltage-gated sodium channel platform for cardiac gene therapy.Nature communications · 2022Article
- Benefits of SGLT2 inhibitors in arrhythmias.Frontiers in cardiovascular medicine · 2022Review
11 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
5 authors at 3 institutions in 1 country.
Funding
Abstract
This review presents the roles of cardiac sodium channel NaV1.5 late current (late INa) in generation of arrhythmic activity. The assumption of the authors is that proper Na(+) channel function is necessary to the maintenance of the transmembrane electrochemical gradient of Na(+) and regulation of cardiac electrical activity. Myocyte Na(+) channels' openings during the brief action potential upstroke contribute to peak INa and initiate excitation-contraction coupling. Openings of Na(+) channels outside the upstroke contribute to late INa, a depolarizing current that persists throughout the action potential plateau. The small, physiological late INa does not appear to be critical for normal electrical or contractile function in the heart. Late INa does, however, reduce the net repolarizing current, prolongs action potential duration, and increases cellular Na(+) loading. An increase of late INa, due to acquired conditions (e.g. heart failure) or inherited Na(+) channelopathies, facilitates the formation of early and delayed afterpolarizations and triggered arrhythmias, spontaneous diastolic depolarization, and cellular Ca(2+) loading. These in turn increase the spatial and temporal dispersion of repolarization time and may lead to reentrant arrhythmias.
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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.