ReviewHandbook of experimental pharmacology2014
The role of late I Na in development of cardiac arrhythmias.
Review in Handbook of experimental pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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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
68 citing papers in PubMed, 146 citations in OpenAlex.
- Late IMedicinal research reviews · 2026Review
- SGLT2 Inhibitor Dapagliflozin Attenuates Cardiomyocyte Injury and Inflammation Induced by PI3Kα-Selective Inhibitor Alpelisib and Fulvestrant Under Hyperglycemia.International journal of molecular sciences · 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
- Gene Therapies in Atrial Fibrillation.Journal of cardiovascular translational research · 2025Review
- Structural basis of human NaProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Propionic Acidemia-Induced Proarrhythmic Electrophysiological Alterations in Human iPSC-Derived Cardiomyocytes.Journal of inherited metabolic disease · 2025Article
- Characterization of novel arrhythmogenic patterns arising secondary to heterogeneous expression and activation of Nav1.8.Frontiers in cardiovascular medicine · 2025Article
- Gene therapy for atrial fibrillation.Journal of molecular and cellular cardiology · 2024Review
- Enhanced Late IInternational journal of molecular sciences · 2024Article
- Prokaryotic voltage-gated sodium channels are more effective than endogenous NaAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- SGLT2 inhibitor ertugliflozin decreases elevated intracellular sodium, and improves energetics and contractile function in diabetic cardiomyopathy.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- Caveolin-3 and Caveolae regulate ventricular repolarization.Journal of molecular and cellular cardiology · 2023Article
- Review
- Increased Density of Endogenous Adenosine AInternational journal of molecular sciences · 2023Article
- Anti-malarial drugs: Mechanisms underlying their proarrhythmic effects.British journal of pharmacology · 2022Review
- Association between Empagliflozin Use and Electrocardiographic Changes.Clinics and practice · 2022Article
- Fibroblast growth factor homologous factors serve as a molecular rheostat in tuning arrhythmogenic cardiac late sodium current.Nature cardiovascular research · 2022Article
- Hypochlorite-Modified LDL Induces Arrhythmia and Contractile Dysfunction in Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2021Article
- Late sodium current and calcium homeostasis in arrhythmogenesis.Channels (Austin, Tex.) · 2021Review
- Ventricular voltage-gated ion channels: Detection, characteristics, mechanisms, and drug safety evaluation.Clinical and translational medicine · 2021Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Late I Na is an integral part of the sodium current, which persists long after the fast-inactivating component. The magnitude of the late I Na is relatively small in all species and in all types of cardiomyocytes as compared with the amplitude of the fast sodium current, but it contributes significantly to the shape and duration of the action potential. This late component had been shown to increase in several acquired or congenital conditions, including hypoxia, oxidative stress, and heart failure, or due to mutations in SCN5A, which encodes the α-subunit of the sodium channel, as well as in channel-interacting proteins, including multiple β subunits and anchoring proteins. Patients with enhanced late I Na exhibit the type-3 long QT syndrome (LQT3) characterized by high propensity for the life-threatening ventricular arrhythmias, such as Torsade de Pointes (TdP), as well as for atrial fibrillation. There are several distinct mechanisms of arrhythmogenesis due to abnormal late I Na, including abnormal automaticity, early and delayed after depolarization-induced triggered activity, and dramatic increase of ventricular dispersion of repolarization. Many local anesthetic and antiarrhythmic agents have a higher potency to block late I Na as compared with fast I Na. Several novel compounds, including ranolazine, GS-458967, and F15845, appear to be the most selective inhibitors of cardiac late I Na reported to date. Selective inhibition of late I Na is expected to be an effective strategy for correcting these acquired and congenital channelopathies.
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Registered trials
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