ReviewNature reviews. Cardiology2012
Potassium-channel mutations and cardiac arrhythmias--diagnosis and therapy.
Review in Nature reviews. Cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 99 citations in OpenAlex.
- Potassium-Selective Nanoelectrode Arrays for Single-Cell Profiling of Human iPSC-Derived Cardiomyocytes.ACS nano · 2026Article
- Primary aldosteronism.Nature reviews. Disease primers · 2026Review
- Stress-Induced Down-Regulation of CPEB4 Disrupts Sodium Channel Regulation and Myocardial Excitability.JACC. Basic to translational science · 2026Article
- Functional Characterization of the SCN5A p.D372H Variant Associated with Brugada Syndrome.Biomedicines · 2026Article
- Low-dimensional materials for intracellular electrophysiology: advances from synthesis to applications.Microsystems & nanoengineering · 2026Review
- High-Throughput Methods for Variant Functional Assessment in Cardiac Disease.Circulation. Genomic and precision medicine · 2026Review
- The impact of the PI3K/AKT pathway on arrhythmia: mechanisms of action and therapeutic potential.Journal of molecular histology · 2026Review
- Modulatory Impact of Oxidative Stress on Action Potentials in Pathophysiological States: A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2024Review
- Review
- Kv beta complex facilitates exercise-induced augmentation of myocardial perfusion and cardiac growth.Frontiers in cardiovascular medicine · 2024Article
- Real-time prognostic biomarkers for predicting in-hospital mortality and cardiac complications in COVID-19 patients.PLOS global public health · 2024Article
- Review
- Dosage of the pseudoautosomal gene SLC25A6 is implicated in QTc interval duration.Scientific reports · 2023Article
- Gene mutations in comorbidity of epilepsy and arrhythmia.Journal of neurology · 2023Review
- Spironolactone as a Potential New Treatment to Prevent Arrhythmias in Arrhythmogenic Cardiomyopathy Cell Model.Journal of personalized medicine · 2023Article
- A Novel DLG1 Variant in a Family with Brugada Syndrome: Clinical Characteristics and In Silico Analysis.Genes · 2023Article
- Diabetes-induced changes in cardiac voltage-gated ion channels.World journal of diabetes · 2021Review
- Impact of arrhythmogenic calmodulin variants on small conductance CaPhysiological reports · 2019Article
- Lamin A mutation impairs interaction with nucleoporin NUP155 and disrupts nucleocytoplasmic transport in atrial fibrillation.Human mutation · 2019Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The coordinated generation and propagation of action potentials within cardiomyocytes creates the intrinsic electrical stimuli that are responsible for maintaining the electromechanical pump function of the human heart. The synchronous opening and closing of cardiac Na(+), Ca(2+), and K(+) channels corresponds with the activation and inactivation of inward depolarizing (Na(+) and Ca(2+)) and outward repolarizing (K(+)) currents that underlie the various phases of the cardiac action potential (resting, depolarization, plateau, and repolarization). Inherited mutations in pore-forming α subunits and accessory β subunits of cardiac K(+) channels can perturb the atrial and ventricular action potential and cause various cardiac arrhythmia syndromes, including long QT syndrome, short QT syndrome, Brugada syndrome, and familial atrial fibrillation. In this Review, we summarize the current understanding of the molecular and cellular mechanisms that underlie K(+)-channel-mediated arrhythmia syndromes. We also describe translational advances that have led to the emerging role of genetic testing and genotype-specific therapy in the diagnosis and clinical management of individuals who harbor pathogenic mutations in genes that encode α or β subunits of cardiac K(+) channels.
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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.