ReviewPflugers Archiv : European journal of physiology2010
Cardiac sodium channelopathies.
Review in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03182777 (Safety of Local Dental Anesthesia in Patients With Cardiac Channelopathies), which is not on this map. Cited by 91 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.
Safety of Local Dental Anesthesia in Patients With Cardiac Channelopathies
Who cites it
91 citing papers in PubMed, 2 syntheses or guidelines pooled it, 211 citations in OpenAlex.
- Variability in reported midpoints of (in)activation of cardiac INa.The Journal of general physiology · 2025Pooled it
- Effectiveness of beta-blockers depending on the genotype of congenital long-QT syndrome: A meta-analysis.PloS one · 2017Pooled it
- Review
- Article
- Subchronic PAH Exposure Impacts Cardiac Electrophysiology of the Polar Fish, Navaga Cod (Toxics · 2026Article
- Selective inhibition of LY294002 across cloned human cardiac ion channels: implications for atrium-selective therapy in atrial fibrillation.Frontiers in pharmacology · 2026Article
- ETV1 orchestrates a self-reinforcing ERK1/2-RSK3 signaling loop to drive atrial fibrillation pathogenesis: implications for targeted therapy.Scientific reports · 2025Article
- Mutation-specific roles of sustained sodium current (IPNAS nexus · 2025Article
- Understanding Brugada Pattern in Elderly Patients with COVID-19: A Case Study.The American journal of case reports · 2025Article
- Charge Reversal of the Uppermost Arginine in Sliding Helix S4-I Affects Gating of Cardiac Sodium Channel.International journal of molecular sciences · 2025Article
- [Reversibility of a critical intraventricular conduction delay under flecainide and lacosamide by sodium bicarbonate].Innere Medizin (Heidelberg, Germany) · 2024Article
- Multisite Validation of a Functional Assay to AdjudicateCirculation. Genomic and precision medicine · 2024Article
- Management of Long QT Syndrome: A Systematic Review.Cureus · 2024Review
- Cardiac GR Mediates the Diurnal Rhythm in Ventricular Arrhythmia Susceptibility.Circulation research · 2024Article
- Biophysical mechanisms of myocardium sodium channelopathies.Pflugers Archiv : European journal of physiology · 2024Review
- HAND factors regulate cardiac lineage commitment and differentiation from human pluripotent stem cells.Stem cell research & therapy · 2024Article
- Multi-site validation of a functional assay to adjudicatemedRxiv : the preprint server for health sciences · 2023Article
- The opioid tramadol blocks the cardiac sodium channel Nav1.5 in HEK293 cells.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023Article
- [Asymptomatic channelopathies : Risk stratification and primary prophylaxis].Herzschrittmachertherapie & Elektrophysiologie · 2023Review
- The Anti-Epileptic Drugs Lamotrigine and Valproic Acid Reduce the Cardiac Sodium Current.Biomedicines · 2023Article
31 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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac sodium channel are protein complexes that are expressed in the sarcolemma of cardiomyocytes to carry a large inward depolarizing current (INa) during phase 0 of the cardiac action potential. The importance of INa for normal cardiac electrical activity is reflected by the high incidence of arrhythmias in cardiac sodium channelopathies, i.e., arrhythmogenic diseases in patients with mutations in SCN5A, the gene responsible for the pore-forming ion-conducting alpha-subunit, or in genes that encode the ancillary beta-subunits or regulatory proteins of the cardiac sodium channel. While clinical and genetic studies have laid the foundation for our understanding of cardiac sodium channelopathies by establishing links between arrhythmogenic diseases and mutations in genes that encode various subunits of the cardiac sodium channel, biophysical studies (particularly in heterologous expression systems and transgenic mouse models) have provided insights into the mechanisms by which INa dysfunction causes disease in such channelopathies. It is now recognized that mutations that increase INa delay cardiac repolarization, prolong action potential duration, and cause long QT syndrome, while mutations that reduce INa decrease cardiac excitability, reduce electrical conduction velocity, and induce Brugada syndrome, progressive cardiac conduction disease, sick sinus syndrome, or combinations thereof. Recently, mutation-induced INa dysfunction was also linked to dilated cardiomyopathy, atrial fibrillation, and sudden infant death syndrome. This review describes the structure and function of the cardiac sodium channel and its various subunits, summarizes major cardiac sodium channelopathies and the current knowledge concerning their genetic background and underlying molecular mechanisms, and discusses recent advances in the discovery of mutation-specific therapies in the management of these channelopathies.
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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.