ReviewBioMed research international2015
Atrial Fibrillation and Fibrosis: Beyond the Cardiomyocyte Centric View.
Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Collagen Prolyl 4-Hydroxylase: An Emerging Key Player in Cardiac Fibrosis.Journal of cardiovascular translational research · 2026Review
- Prediction of arrhythmogenesis in non-ischemic cardiac resynchronization therapy patients.APL bioengineering · 2026Article
- Association between T cell exhaustion and the recurrence of atrial fibrillation after cryoballoon ablation.Frontiers in immunology · 2026Article
- Left Atrial Mechanics and Remodeling in Paroxysmal Atrial Fibrillation: Introducing the EASE Score for Pre-Ablation Risk Prediction.Medical sciences (Basel, Switzerland) · 2025Article
- Inflammatory and fibrotic signaling pathways mediated by cardiac macrophages in atrial fibrillation.Frontiers in cardiovascular medicine · 2025Review
- Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis.Journal of molecular and cellular cardiology · 2024Review
- Sacubitril/valsartan attenuates atrial conduction disturbance and electrophysiological heterogeneity with ameliorating fibrosis in mice.Frontiers in cardiovascular medicine · 2024Article
- The Effects of Fibrotic Cell Type and Its Density on Atrial Fibrillation Dynamics: An In Silico Study.Cells · 2021Article
- The matricellular protein CCN5 prevents adverse atrial structural and electrical remodelling.Journal of cellular and molecular medicine · 2020Article
- The Therapeutic Potential of MicroRNAs in Atrial Fibrillation.Mediators of inflammation · 2020Review
- Identification of atrial fibrillation associated genes and functional non-coding variants.Nature communications · 2019Article
- Addressing challenges of quantitative methodologies and event interpretation in the study of atrial fibrillation.Computer methods and programs in biomedicine · 2019Review
- Sacubitril/Valsartan Improves Left Atrial and Left Atrial Appendage Function in Patients With Atrial Fibrillation and in Pressure Overload-Induced Mice.Frontiers in pharmacology · 2019Article
- Atrial fibrosis: an obligatory component of arrhythmia mechanisms in atrial fibrillation?Journal of geriatric cardiology : JGC · 2017Article
- Atrial structure, function and arrhythmogenesis in aged and frail mice.Scientific reports · 2017Article
- Atrial fibrosis: an obligatory component of arrhythmia mechanisms in atrial fibrillation?Journal of geriatric cardiology : JGC · 2017Article
- Atrial Fibrillation Dynamics and Ionic Block Effects in Six Heterogeneous Human 3D Virtual Atria with Distinct Repolarization Dynamics.Frontiers in bioengineering and biotechnology · 2017Article
- The impacts of age and frailty on heart rate and sinoatrial node function.The Journal of physiology · 2016Article
- Age is just a number: frailty better evaluates age-dependent heart rhythm defects.The Journal of physiology · 2016Article
- Calcium Sparks in the Heart: Dynamics and Regulation.Research and reports in biologyArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrillation (AF) associated with fibrosis is characterized by the appearance of interstitial myofibroblasts. These cells are responsible for the uncontrolled deposition of the extracellular matrix, which pathologically separate cardiomyocyte bundles. The enhanced fibrosis is thought to contribute to arrhythmias "indirectly" because a collagenous septum is a passive substrate for propagation, resulting in impulse conduction block and/or zigzag conduction. However, the emerging results demonstrate that myofibroblasts in vitro also promote arrhythmogenesis due to direct implications upon cardiomyocyte electrophysiology. This electrical interference may be considered beneficial as it resolves any conduction blocks; however, the passive properties of myofibroblasts might cause a delay in impulse propagation, thus promoting AF due to discontinuous slow conduction. Moreover, low-polarized myofibroblasts reduce, via cell-density dependence, the fast driving inward current for cardiac impulse conduction, therefore resulting in arrhythmogenic uniformly slow propagation. Critically, the subsequent reduction in cardiomyocytes resting membrane potential in vitro significantly increases the likelihood of ectopic activity. Myofibroblast densities and the degree of coupling at cellular border zones also impact upon this likelihood. By considering future in vivo studies, which identify myofibroblasts "per se" as a novel targets for cardiac arrhythmias, this review aims to describe the implications of noncardiomyocyte view in the context 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.