ReviewBiology2022
Atrial Fibrillation: Focus on Myocardial Connexins and Gap Junctions.
Review in Biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 34 citations in OpenAlex.
- Propafenone-mediated gap junctional uncoupling results from aberrant connexin-43 trafficking.Pharmacological reports : PR · 2026Article
- A New Paradigm for Atrial Fibrillation Ablation in Obesity Focusing on Substrate Remodeling and Patient-Centered Outcomes.Reviews in cardiovascular medicine · 2026Review
- Gap junctional and ephaptic coupling in cardiac electrical propagation: homocellular and heterocellular perspectives.The Journal of physiology · 2026Review
- Ionic Disorders in Persistent Atrial Fibrillation: Therapeutic Targeting by Plant-Derived Bioactive Compounds.Cardiology research and practice · 2026Review
- Macrophage migration inhibitory factor in atrial fibrillation.Frontiers in immunology · 2026Review
- Genetic loci responsible for atrioventricular block in children.Frontiers in cell and developmental biology · 2026Review
- Molecular Mechanisms of Atrial Fibrillation Recurrence After Successful Catheter Ablation.Cells · 2025Review
- Atrial fibrillation: from pathogenesis to novel treatment options.Molecular biomedicine · 2025Review
- Gene Therapies in Atrial Fibrillation.Journal of cardiovascular translational research · 2025Review
- Connexin 40 in atrial fibrillation: pathophysiological roles and regulatory mechanisms.Annals of medicine · 2025Review
- Brazilian Atrial Fibrillation Guidelines - 2025.Arquivos brasileiros de cardiologia · 2025Article
- Low-intensity pulsed ultrasound attenuates atrial remodelling and atrial fibrillation after myocardial infarction: an experimental pre-clinical study.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 · 2025Article
- Hybrid Ablation in Atrial Fibrillation: Bridging Mechanistic Understanding and Clinical Practice.Journal of cardiovascular development and disease · 2025Review
- N-palmitoyl glycine mediates depression-associated atrial fibrillation via Man1a2-dependent autophagy and NRAP dysregulation.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 · 2025Article
- EXPRESSION OF CONNEXIN-40 AND INTERLEUKIN 6 GENES IN PATIENTS WITH ATRIAL FIBRILLATION.Acta clinica Croatica · 2025Article
- Research progress of connexin 43 in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- Cardiac Fibroblasts Enhance MMP2 Activity to Suppress Gap Junction Function in Cardiomyocytes.Applied biochemistry and biotechnology · 2024Article
- Identification and Functional Investigation ofDiagnostics (Basel, Switzerland) · 2024Article
- Effects of Heart Failure Therapies on Atrial Fibrillation: Biological and Clinical Perspectives.Antioxidants (Basel, Switzerland) · 2024Review
- Arrhythmic Effects Evaluated onACS nano · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrillation (AF) represents the most common type of clinical cardiac arrhythmia worldwide and contributes to substantial morbidity, mortality and socioeconomic burden. Aggregating evidence highlights the strong genetic basis of AF. In addition to chromosomal abnormalities, pathogenic mutations in over 50 genes have been causally linked to AF, of which the majority encode ion channels, cardiac structural proteins, transcription factors and gap junction channels. In the heart, gap junctions comprised of connexins (Cxs) form intercellular pathways responsible for electrical coupling and rapid coordinated action potential propagation between adjacent cardiomyocytes. Among the 21 isoforms of connexins already identified in the mammal genomes, 5 isoforms (Cx37, Cx40, Cx43, Cx45 and Cx46) are expressed in human heart. Abnormal electrical coupling between cardiomyocytes caused by structural remodeling of gap junction channels (alterations in connexin distribution and protein levels) has been associated with enhanced susceptibility to AF and recent studies have revealed multiple causative mutations or polymorphisms in 4 isoforms of connexins predisposing to AF. In this review, an overview of the genetics of AF is made, with a focus on the roles of mutant myocardial connexins and gap junctions in the pathogenesis of AF, to underscore the hypothesis that cardiac connexins are a major molecular target in the management of AF.
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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.