ArticleHeart rhythm2013
Inhibition of platelet-derived growth factor-AB signaling prevents electromechanical remodeling of adult atrial myocytes that contact myofibroblasts.
Article in Heart rhythm, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 3 of them syntheses that pooled it.
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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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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
28 citing papers in PubMed, 3 syntheses or guidelines pooled it, 55 citations in OpenAlex.
- Atrial Fibrillation Recurrence Risk After Catheter Ablation in Patients With Rheumatoid Arthritis: A Systematic Review and Meta-Analysis.Clinical cardiology · 2025Pooled it
- Modulated Calcium Homeostasis and Release Events Under Atrial Fibrillation and Its Risk Factors: A Meta-Analysis.Frontiers in cardiovascular medicine · 2021Pooled it
- Pooled it
- The mechanism of electrical remodeling in atrial fibrillation and current research status of natural drugs and active ingredients inhibiting atrial electrical remodeling.Frontiers in cardiovascular medicine · 2026Review
- Psoriasis and atrial fibrillation: Exploring the intersection.World journal of experimental medicine · 2025Review
- Preoperative Activation of c-Src Kinase in Atrial Tissue in Patients Developing Postoperative Atrial Fibrillation.Medicina (Kaunas, Lithuania) · 2025Article
- Immune cells and arrhythmias.Cardiovascular research · 2025Review
- Interactions between atrial fibrosis and inflammation in atrial fibrillation.Frontiers in cardiovascular medicine · 2025Review
- Transcriptional Dysregulation Underlies Both Monogenic Arrhythmia Syndrome and Common Modifiers of Cardiac Repolarization.Circulation · 2023Article
- Characteristics of immune clusters and cell abundance in patients with different subtypes of nonparoxysmal atrial fibrillation.Scientific reports · 2023Article
- Effects of Inflammatory Cell Death Caused by Catheter Ablation on Atrial Fibrillation.Journal of inflammation research · 2023Review
- PDGF/PDGFR: A Possible Molecular Target in Scleroderma Fibrosis.International journal of molecular sciences · 2022Review
- Influenza vaccination and risk of atrial fibrillation in patients with gout: A nationwide population-based cohort study.Frontiers in pharmacology · 2022Article
- Regional Diversities in Fibrogenesis Weighed as a Key Determinant for Atrial Arrhythmogenesis.Biomedicines · 2021Review
- Atrial fibrillation: the role of hypoxia-inducible factor-1-regulated cytokines.Molecular and cellular biochemistry · 2021Review
- Burden of atrial fibrillation in patients with rheumatic diseases.World journal of clinical cases · 2021Article
- Role of PDGF-A/B Ligands in Cardiac Repair After Myocardial Infarction.Frontiers in cell and developmental biology · 2021Review
- AGE-RAGE Stress in the Pathophysiology of Atrial Fibrillation and Its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2020Article
- Enhanced cardiomyocyte reactive oxygen species signaling promotes ibrutinib-induced atrial fibrillation.Redox biology · 2020Article
- The expression profile analysis of atrial mRNA in rats with atrial fibrillation: the role of IGF1 in atrial fibrosis.BMC cardiovascular disorders · 2019Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPersistent atrial fibrillation (PAF) results in electromechanical and structural remodeling by mechanisms that are poorly understood. Myofibroblast proliferation and fibrosis are major sources of structural remodeling in PAF. Myofibroblasts also interact with atrial myocytes via direct physical contact and release of signaling molecules, which may contribute to remodeling.
objectiveTo determine whether myofibroblasts contribute to atrial myocyte electromechanical remodeling via direct physical contact and platelet-derived growth factor (PDGF) signaling.
methodsMyofibroblasts and myocytes from adult sheep atria were co-cultured for 24 hours. Alternatively adult sheep atrial myocytes were exposed to 1 ng/mL recombitant PDGF AB peptide for 24 hours.
resultsMyocytes making contact with myofibroblasts demonstrated significant reduction (P ≤ .05) in peak L-type calcium current density, shortening of action potential duration (APD), and reduction in calcium transients. These effects were blocked by pretreatment with a PDGF-AB neutralizing anti-body. Heterocellular contact also severely disturbed the localization of the L-type calcium channel. Myocytes exposed to recombinant PDGF-AB peptide for 24 hours demonstrated reduced APD50, APD80 and Peak L-type calcium current. Pretreatment with a PDGF-AB neutralizing antibody prevented these effects. Finally, while control atrial myocytes did not respond in a 1:1 manner to pacing frequencies of 3 Hz or higher, atrial myocytes from hearts that were tachypaced for 2 months and normal myocytes treated with PDGF-AB for 24 hours could be paced up to 10 Hz.
conclusionsIn addition to leading to fibrosis, atrial myofibroblasts contribute to electromechanical remodeling of myocytes via direct physical contact and release of PDGF-AB, which may be a factor in PAF-induced remodeling.
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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.