ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Atrial fibrillation and sinus node dysfunction in human ankyrin-B syndrome: a computational analysis.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Reappraisal ofReviews in cardiovascular medicine · 2025Review
- Sinoatrial node heterogeneity and fibroblasts increase atrial driving capability in a two-dimensional human computational model.Frontiers in physiology · 2024Article
- Pathophysiology of CaFrontiers in physiology · 2023Review
- Pleiotropic Ankyrins: Scaffolds for Ion Channels and Transporters.Channels (Austin, Tex.) · 2022Review
- Regulation of Cardiac Conduction and Arrhythmias by Ankyrin/Spectrin-Based Macromolecular Complexes.Journal of cardiovascular development and disease · 2021Review
- Genetic Complexity of Sinoatrial Node Dysfunction.Frontiers in genetics · 2021Review
- Loss of insulin signaling may contribute to atrial fibrillation and atrial electrical remodeling in type 1 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Mechanisms and Alterations of Cardiac Ion Channels Leading to Disease: Role of Ankyrin-B in Cardiac Function.Biomolecules · 2020Review
- The Cardiac Pacemaker Story-Fundamental Role of the NaFrontiers in pharmacology · 2020Review
- Understanding the Beat-to-Beat Variations of P-Waves Morphologies in AF Patients During Sinus Rhythm: A Scoping Review of the Atrial Simulation Studies.Frontiers in physiology · 2019Article
- The evolving role of ankyrin-B in cardiovascular disease.Heart rhythm · 2017Review
- CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Atrial structure, function and arrhythmogenesis in aged and frail mice.Scientific reports · 2017Article
- Towards personalized computational modelling of the fibrotic substrate for atrial arrhythmia.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 · 2016Review
- Patient-derived models link re-entrant driver localization in atrial fibrillation to fibrosis spatial pattern.Cardiovascular research · 2016Article
- Two-Pore K+ Channel TREK-1 Regulates Sinoatrial Node Membrane Excitability.Journal of the American Heart Association · 2016Article
- Article
- Human sinoatrial node structure: 3D microanatomy of sinoatrial conduction pathways.Progress in biophysics and molecular biology · 2016Article
- Malignant systemic hypertension, encephalopathy and bradycardia following splenectomy for hereditary spherocytosis.BMJ case reports · 2015Article
- Function and dysfunction of human sinoatrial node.Korean circulation journal · 2015Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Ankyrin-B is a multifunctional adapter protein responsible for localization and stabilization of select ion channels, transporters, and signaling molecules in excitable cells including cardiomyocytes. Ankyrin-B dysfunction has been linked with highly penetrant sinoatrial node (SAN) dysfunction and increased susceptibility to atrial fibrillation. While previous studies have identified a role for abnormal ion homeostasis in ventricular arrhythmias, the molecular mechanisms responsible for atrial arrhythmias and SAN dysfunction in human patients with ankyrin-B syndrome are unclear. Here, we develop a computational model of ankyrin-B dysfunction in atrial and SAN cells and tissue to determine the mechanism for increased susceptibility to atrial fibrillation and SAN dysfunction in human patients with ankyrin-B syndrome. Our simulations predict that defective membrane targeting of the voltage-gated L-type Ca(2+) channel Cav1.3 leads to action potential shortening that reduces the critical atrial tissue mass needed to sustain reentrant activation. In parallel, increased fibrosis results in conduction slowing that further increases the susceptibility to sustained reentry in the setting of ankyrin-B dysfunction. In SAN cells, loss of Cav1.3 slows spontaneous pacemaking activity, whereas defects in Na(+)/Ca(2+) exchanger and Na(+)/K(+) ATPase increase variability in SAN cell firing. Finally, simulations of the intact SAN reveal a shift in primary pacemaker site, SAN exit block, and even SAN failure in ankyrin-B-deficient tissue. These studies identify the mechanism for increased susceptibility to atrial fibrillation and SAN dysfunction in human disease. Importantly, ankyrin-B dysfunction involves changes at both the cell and tissue levels that favor the common manifestation of atrial arrhythmias and SAN dysfunction.
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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.