ReviewPediatric cardiology2012
Cardiac sodium channel Nav1.5 mutations and cardiac arrhythmia.
Review in Pediatric cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 62 citations in OpenAlex.
- Dihydrosanguinarine: A Review of Its Pharmacology, Structure-Activity Relationship, Toxicity, Pharmacokinetics, and Clinical Prospects.International journal of molecular sciences · 2026Review
- Targeting the Ubiquitin-Proteasome System in Atrial Fibrillation: Mechanistic Insights and Translational Perspectives.Current issues in molecular biology · 2025Review
- Investigating the role of the I-II linker in Nav1.5 channel function.The Journal of general physiology · 2025Article
- Consequences of Right Heart Disease for Cardiac Electrophysiology and Arrhythmias: Cellular and Structural Mechanisms.CJC open · 2025Review
- Mitochondrial Transport Proteins in Cardiovascular Diseases: Metabolic Gatekeepers, Pathogenic Mediators and Therapeutic Targets.International journal of molecular sciences · 2025Review
- Voltage-gated sodium channels in excitable cells as drug targets.Nature reviews. Drug discovery · 2025Review
- Heart Failure and Arrhythmias: Circadian and Epigenetic Interplay in Myocardial Electrophysiology.International journal of molecular sciences · 2025Review
- A novel gain-of-function mutationAmerican journal of cardiovascular disease · 2025Article
- Advancements in Non-Addictive Analgesic Diterpenoid Alkaloid Lappaconitine: A Review.International journal of molecular sciences · 2024Review
- Dynamic Changes in Ion Channels during Myocardial Infarction and Therapeutic Challenges.International journal of molecular sciences · 2024Review
- Opioids-Induced Long QT Syndrome: A Challenge to Cardiac Health.Cardiovascular toxicology · 2024Review
- Long QT syndrome-associated calmodulin variants disrupt the activity of the slowly activating delayed rectifier potassium channel.The Journal of physiology · 2023Article
- Pharmacological Features of 18β-Glycyrrhetinic Acid: A Pentacyclic Triterpenoid of Therapeutic Potential.Plants (Basel, Switzerland) · 2023Review
- Inhibition of late sodium current via PI3K/Akt signaling prevents cellular remodeling in tachypacing-induced HL-1 atrial myocytes.Pflugers Archiv : European journal of physiology · 2023Article
- Acute osimertinib exposure induces electrocardiac changes by synchronously inhibiting the currents of cardiac ion channels.Frontiers in pharmacology · 2023Article
- Roles of stretch-activated channels and NADPH oxidase 2 in the induction of twitch contraction by muscle stretching in rat ventricular muscle.Pflugers Archiv : European journal of physiology · 2022Article
- Genomic and Non-Genomic Regulatory Mechanisms of the Cardiac Sodium Channel in Cardiac Arrhythmias.International journal of molecular sciences · 2022Review
- Hypernatremia and intercalated disc edema synergistically exacerbate long-QT syndrome type 3 phenotype.American journal of physiology. Heart and circulatory physiology · 2021Article
- Effective Accentuation of Voltage-Gated Sodium Current Caused by Apocynin (4'-Hydroxy-3'-methoxyacetophenone), a Known NADPH-Oxidase Inhibitor.Biomedicines · 2021Article
- Inhibition of Nav1.7 channel by a novel blocker QLS-81 for alleviation of neuropathic pain.Acta pharmacologica Sinica · 2021Article
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 at 1 institution in 1 country.
Funding
Abstract
As a major cardiac voltage-gated sodium channel isoform in the heart, the Nav1.5 channel is essential for cardiac action potential initiation and subsequent propagation throughout the heart. Mutations of Nav1.5 have been linked to a variety of cardiac diseases such as long QT syndrome (LQTs), Brugada syndrome, cardiac conduction defect, atrial fibrillation, and dilated cardiomyopathy. The mutagenesis approach and heterologous expression systems are most frequently used to study the function of this channel. This review focuses primarily on recent findings of Nav1.5 mutations associated with type 3 long QT syndrome (LQT3) in particular. Understanding the functional changes of the Nav1.5 mutation may offer critical insight into the mechanism of long QT3 syndrome. In addition, this review provides the updated information on the current progress of using various experimental model systems to study primarily the long QT3 syndrome.
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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.