ArticleCirculation research2010
Enhanced fibroblast-myocyte interactions in response to cardiac injury.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
What it found
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Who cites it
103 citing papers in PubMed.
- Towards mechanisms-driven strategy for persistent atrial fibrillation ablation: Leveraging digital twins.Journal of precision medicine (Amsterdam, Netherlands) · 2026Article
- Connexin-43 Restoration Alleviates Desmosomal Arrhythmogenic Cardiomyopathy.Circulation. Heart failure · 2026Article
- Heart failure-specific cardiac fibroblasts contribute to cardiac dysfunction via the MYC-CXCL1-CXCR2 axis.Nature cardiovascular research · 2025Article
- TGF-β-Driven Atrial Fibrosis in Atrial Fibrillation: From Mechanistic Insights to Targeted Therapies.Aging and disease · 2025Review
- Unraveling the Complex Cellular Repair Mechanisms Following Myocardial Infarction.International journal of molecular sciences · 2025Review
- Harnessing native blueprints for designing bioinks to bioprint functional cardiac tissue.iScience · 2025Review
- The epigenetic regulation of crosstalk between cardiac fibroblasts and other cardiac cell types during stress.Frontiers in cardiovascular medicine · 2025Review
- Hypoxic-Normoxic Crosstalk Activates Pro-Inflammatory Signaling in Human Cardiac Fibroblasts and Myocytes in a Post-Infarct Myocardium on a Chip.Advanced healthcare materials · 2024Article
- Distinct phenotypes induced by acute hypoxia and TGF-β1 in human adult cardiac fibroblasts.Journal of molecular and cellular cardiology plus · 2024Article
- Review
- Ferroptosis in diabetic cardiomyopathy: Advances in cardiac fibroblast-cardiomyocyte interactions.Heliyon · 2024Review
- The role of cardiac microenvironment in cardiovascular diseases: implications for therapy.Human cell · 2024Review
- Cardiomyocyte-fibroblast interaction regulates ferroptosis and fibrosis after myocardial injury.iScience · 2024Article
- Fibroblasts under pressure: cardiac fibroblast responses to hypertension and antihypertensive therapies.American journal of physiology. Heart and circulatory physiology · 2024Review
- Article
- Epigenetic Regulation of Fibroblasts and Crosstalk between Cardiomyocytes and Non-Myocyte Cells in Cardiac Fibrosis.Biomolecules · 2023Review
- Human myofibroblasts increase the arrhythmogenic potential of human induced pluripotent stem cell-derived cardiomyocytes.Cellular and molecular life sciences : CMLS · 2023Article
- Nonmyocytes as electrophysiological contributors to cardiac excitation and conduction.American journal of physiology. Heart and circulatory physiology · 2023Review
- Chronic activation of human cardiac fibroblasts in vitro attenuates the reversibility of the myofibroblast phenotype.Scientific reports · 2023Article
- COVID-19 HEART unveiling as atrial fibrillation: pathophysiology, management and future directions for research.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2023Review
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
rationaleA critical event in the development of cardiac fibrosis is the transformation of fibroblasts into myofibroblasts. The electrophysiological consequences of this phenotypic switch remain largely unknown.
objectiveDetermine whether fibroblast activation following cardiac injury results in a distinct electrophysiological phenotype that enhances fibroblast-myocyte interactions. METHODS AND
resultsNeonatal rat myocyte monolayers were treated with media (CM) conditioned by fibroblasts isolated from normal (Fb) and infarcted (MI-Fb) hearts. Fb and MI-Fb were also plated on top of myocyte monolayers at 3 densities. Cultures were optically mapped after CM treatment or fibroblast plating to obtain conduction velocity and action potential duration (APD(70)). Intercellular communication and connexin43 expression levels were assessed. Membrane properties of Fb and MI-Fb were evaluated using patch clamp techniques. MI-Fb CM treatment decreased conduction velocity (11.1%) compared to untreated myocyte cultures. APD(70) was reduced by MI-Fb CM treatment compared to homocellular myocyte culture (9.4%) and Fb CM treatment (6.4%). In heterocellular cultures, MI-Fb conduction velocities were different from Fb at all densities (+29.8%, -23.0%, and -16.7% at 200, 400, and 600 cells/mm(2), respectively). APD(70) was reduced (9.6%) in MI-Fb compared to Fb cultures at 200 cells/mm(2). MI-Fb had more hyperpolarized resting membrane potentials and increased outward current densities. Connexin43 was elevated (134%) in MI-Fb compared to Fb. Intercellular coupling evaluated with gap fluorescence recovery after photobleaching was higher between myocytes and MI-Fb compared to Fb.
conclusionsThese data demonstrate cardiac injury results in significant electrophysiological changes that enhance fibroblast-myocyte interactions and could contribute to the greater incidence of arrhythmias observed in fibrotic hearts.
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Registered trials
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