ArticlePLoS computational biology2014
In silico screening of the key cellular remodeling targets in chronic atrial fibrillation.
Article in PLoS computational biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 68 citations in OpenAlex.
- Catheter configuration for mapping micro-anatomic reentries sustaining atrial fibrillation: A simulation study.PLoS computational biology · 2026Article
- Influence of Anatomical Definition and Substrate Condition on Simulations of Atrial Arrhythmias.Annals of biomedical engineering · 2026Article
- Computational modeling of cardiac electrophysiology and arrhythmogenesis: toward clinical translation.Physiological reviews · 2024Review
- Human induced pluripotent stem cell-derived atrial cardiomyocytes recapitulate contribution of the slowly activating delayed rectifier currents IKs to repolarization in the human atrium.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 · 2024Article
- Caveolin-3 and Caveolin-1 Interaction Decreases Channel Dysfunction Due to Caveolin-3 Mutations.International journal of molecular sciences · 2024Article
- Rotors Drift Toward and Stabilize in Low Power Regions in Heterogeneous Models of Atrial Fibrillation.Computing in cardiology · 2022Article
- Novel insights into the electrophysiology of murine cardiac macrophages: relevance of voltage-gated potassium channels.Cardiovascular research · 2022Article
- Understanding PITX2-Dependent Atrial Fibrillation Mechanisms through Computational Models.International journal of molecular sciences · 2021Review
- Computational models of atrial fibrillation: achievements, challenges, and perspectives for improving clinical care.Cardiovascular research · 2021Review
- Non-invasive Estimation of Atrial Fibrillation Driver Position With Convolutional Neural Networks and Body Surface Potentials.Frontiers in physiology · 2021Article
- Immediate and Delayed Response of Simulated Human Atrial Myocytes to Clinically-Relevant Hypokalemia.Frontiers in physiology · 2021Article
- Artificial Intelligence-Driven Algorithm for Drug Effect Prediction on Atrial Fibrillation: AnFrontiers in physiology · 2021Article
- PITX2 upregulation increases the risk of chronic atrial fibrillation in a dose-dependent manner by modulatingAnnals of translational medicine · 2020Article
- Sensitivity and Uncertainty Analysis of Two Human Atrial Cardiac Cell Models Using Gaussian Process Emulators.Frontiers in physiology · 2020Article
- Computational modeling: What does it tell us about atrial fibrillation therapy?International journal of cardiology · 2019Review
- Chaotic tip trajectories of a single spiral wave in the presence of heterogeneities.Physical review. E · 2019Article
- Proarrhythmia in the p.Met207Val PITX2c-Linked Familial Atrial Fibrillation-Insights From Modeling.Frontiers in physiology · 2019Article
- 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
- Heterogeneous Effects of Fibroblast-Myocyte Coupling in Different Regions of the Human Atria Under Conditions of Atrial Fibrillation.Frontiers in physiology · 2019Article
- Computational Modeling of Electrophysiology and Pharmacotherapy of Atrial Fibrillation: Recent Advances and Future Challenges.Frontiers in physiology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic atrial fibrillation (AF) is a complex disease with underlying changes in electrophysiology, calcium signaling and the structure of atrial myocytes. How these individual remodeling targets and their emergent interactions contribute to cell physiology in chronic AF is not well understood. To approach this problem, we performed in silico experiments in a computational model of the human atrial myocyte. The remodeled function of cellular components was based on a broad literature review of in vitro findings in chronic AF, and these were integrated into the model to define a cohort of virtual cells. Simulation results indicate that while the altered function of calcium and potassium ion channels alone causes a pronounced decrease in action potential duration, remodeling of intracellular calcium handling also has a substantial impact on the chronic AF phenotype. We additionally found that the reduction in amplitude of the calcium transient in chronic AF as compared to normal sinus rhythm is primarily due to the remodeling of calcium channel function, calcium handling and cellular geometry. Finally, we found that decreased electrical resistance of the membrane together with remodeled calcium handling synergistically decreased cellular excitability and the subsequent inducibility of repolarization abnormalities in the human atrial myocyte in chronic AF. We conclude that the presented results highlight the complexity of both intrinsic cellular interactions and emergent properties of human atrial myocytes in chronic AF. Therefore, reversing remodeling for a single remodeled component does little to restore the normal sinus rhythm phenotype. These findings may have important implications for developing novel therapeutic approaches for chronic AF.
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