ReviewProgress in biophysics and molecular biology
Late sodium current in failing heart: friend or foe?
Review in Progress in biophysics and molecular biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed.
- Late IMedicinal research reviews · 2026Review
- Optogenetic quantification of cardiac excitability and electrical coupling in intact hearts to explain cardiac arrhythmia initiation.Science advances · 2025Article
- Riluzole is associated with reduced risk of heart failure.European journal of neurology · 2025Article
- NaInternational journal of molecular sciences · 2024Article
- Changes in cellular CaThe Journal of physiology · 2023Article
- Ranolazine - could an antianginal drug be used in stroke prevention?International journal of cardiology. Cardiovascular risk and prevention · 2022Article
- Article
- Late Sodium Current of the Heart: Where Do We Stand and Where Are We Going?Pharmaceuticals (Basel, Switzerland) · 2022Review
- Fibroblast growth factor homologous factors tune arrhythmogenic late NaV1.5 current in calmodulin binding-deficient channels.JCI insight · 2020Article
- Changes in cellular CaThe Journal of physiology · 2020Article
- Ranolazine-Mediated Attenuation of Mechanoelectric Feedback in Atrial Myocyte Monolayers.Frontiers in physiology · 2020Article
- Late Sodium Current Inhibitors as Potential Antiarrhythmic Agents.Frontiers in pharmacology · 2020Review
- Mechanisms and models of cardiac sodium channel inactivation.Channels (Austin, Tex.) · 2017Review
- C-terminal phosphorylation of NaThe Journal of biological chemistry · 2017Article
- Enhanced Late Na and Ca Currents as Effective Antiarrhythmic Drug Targets.Frontiers in pharmacology · 2017Review
- Tolterodine reduces veratridine-augmented late IActa pharmacologica Sinica · 2016Article
- Myocyte repolarization modulates myocardial function in aging dogs.American journal of physiology. Heart and circulatory physiology · 2016Article
- Increased Late Sodium Current Contributes to the Electrophysiological Effects of Chronic, but Not Acute, Dofetilide Administration.Circulation. Arrhythmia and electrophysiology · 2016Article
- Late sodium current: A mechanism for angina, heart failure, and arrhythmia.Trends in cardiovascular medicine · 2016Review
- Recent advances in understanding cardiac contractility in health and disease.F1000Research · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Most cardiac Na+ channels open transiently upon membrane depolarization and then are quickly inactivated. However, some channels remain active, carrying the so-called persistent or late Na+ current (INaL) throughout the action potential (AP) plateau. Experimental data and the results of numerical modeling accumulated over the past decade show the emerging importance of this late current component for the function of both normal and failing myocardium. INaL is produced by special gating modes of the cardiac-specific Na+ channel isoform. Heart failure (HF) slows channel gating and increases INaL, but HF-specific Na+ channel isoform underlying these changes has not been found. Na+ channels represent a multi-protein complex and its activity is determined not only by the pore-forming alpha subunit but also by its auxiliary beta subunits, cytoskeleton, calmodulin, regulatory kinases and phosphatases, and trafficking proteins. Disruption of the integrity of this protein complex may lead to alterations of INaL in pathological conditions. Increased INaL and the corresponding Na+ flux in failing myocardium contribute to abnormal repolarization and an increased cell Ca2+ load. Interventions designed to correct INaL rescue normal repolarization and improve Ca2+ handling and contractility of the failing cardiomyocytes. This review considers (1) quantitative integration of INaL into the established electrophysiological and Ca2+ regulatory mechanisms in normal and failing cardiomyocytes and (2) a new therapeutic strategy utilizing a selective inhibition of INaL to target both arrhythmias and impaired contractility in HF.
Indexed as
Identifiers
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.