ReviewCardiovascular & hematological agents in medicinal chemistry2008
Late sodium current is a new therapeutic target to improve contractility and rhythm in failing heart.
Review in Cardiovascular & hematological agents in medicinal chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- SGLT2 Inhibitor Dapagliflozin Attenuates Cardiomyocyte Injury and Inflammation Induced by PI3Kα-Selective Inhibitor Alpelisib and Fulvestrant Under Hyperglycemia.International journal of molecular sciences · 2026Article
- Ranolazine Unveiled: Rediscovering an Old Solution in a New Light.Journal of clinical medicine · 2024Review
- The potential anti-arrhythmic effect of SGLT2 inhibitors.Cardiovascular diabetology · 2024Review
- Ranolazine: An Old Drug with Emerging Potential; Lessons from Pre-Clinical and Clinical Investigations for Possible Repositioning.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Late sodium current and calcium homeostasis in arrhythmogenesis.Channels (Austin, Tex.) · 2021Review
- Acquired long QT syndrome in chronic kidney disease patients.Renal failure · 2020Review
- Late ICirculation. Arrhythmia and electrophysiology · 2020Article
- Mechanisms of Action of the KCa2-Negative Modulator AP30663, a Novel Compound in Development for Treatment of Atrial Fibrillation in Man.Frontiers in pharmacology · 2020Article
- Late sodium current associated cardiac electrophysiological and mechanical dysfunction.Pflugers Archiv : European journal of physiology · 2018Review
- Barbaloin inhibits ventricular arrhythmias in rabbits by modulating voltage-gated ion channels.Acta pharmacologica Sinica · 2018Article
- Mechanism of Action Potential Prolongation During Metabolic Inhibition in the Whole Rabbit Heart.Frontiers in physiology · 2018Article
- Cardiac Arrhythmias as Manifestations of Nanopathies: An Emerging View.Frontiers in physiology · 2018Review
- Neuronal sodium channels: emerging components of the nano-machinery of cardiac calcium cycling.The Journal of physiology · 2017Review
- Enhanced Late Na and Ca Currents as Effective Antiarrhythmic Drug Targets.Frontiers in pharmacology · 2017Review
- Icariin, a Novel Blocker of Sodium and Calcium Channels, Eliminates Early and Delayed Afterdepolarizations, As Well As Triggered Activity, in Rabbit Cardiomyocytes.Frontiers in physiology · 2017Article
- Tolterodine reduces veratridine-augmented late IActa pharmacologica Sinica · 2016Article
- Late sodium current (INaL) in pancreatic β-cells.Pflugers Archiv : European journal of physiology · 2015Article
- Contribution of sodium channel neuronal isoform Nav1.1 to late sodium current in ventricular myocytes from failing hearts.The Journal of physiology · 2015Article
- Deranged sodium to sudden death.The Journal of physiology · 2015Review
- The role of late I Na in development of cardiac arrhythmias.Handbook of experimental pharmacology · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Most cardiac Na+ channels open transiently within milliseconds upon membrane depolarization and are responsible for the excitation propagation. However, some channels remain active during hundreds of milliseconds, carrying the so-called persistent or late Na+ current (I(NaL)) throughout the action potential plateau. I(NaL) is produced by special gating modes of the cardiac-specific Na+ channel isoform. Experimental data accumulated over the past decade show the emerging importance of this late current component for the function of both normal and especially failing myocardium, where I(NaL) is reportedly increased. 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, and by Ca2+ signaling and trafficking proteins. Remodeling of this protein complex and intracellular signaling pathways may lead to alterations of I(NaL) in pathological conditions. Increased I(NaL) and the corresponding Na+ influx in failing myocardium contribute to abnormal repolarization and an increased cell Ca2+ load. Interventions designed to correct I(NaL) rescue normal repolarization and improve Ca2+ handling and contractility of the failing cardiomyocytes. New therapeutic strategies to target both arrhythmias and deficient contractility in HF may not be limited to the selective inhibition of I(NaL) but also include multiple indirect, modulatory (e.g. Ca(2+)- or cytoskeleton- dependent) mechanisms of I(NaL) function.
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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.