ArticleAmerican journal of physiology. Heart and circulatory physiology2012
Myofibroblasts cause heterogeneous Cx43 reduction and are unlikely to be coupled to myocytes in the healing canine infarct.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 52 citations in OpenAlex.
- Cardioimmunology of Myocarditis: Targeting the IL-1 Pathway.Current cardiology reports · 2026Review
- Interleukin-1β Drives Disease Progression in Arrhythmogenic Cardiomyopathy.JACC. Basic to translational science · 2026Article
- Interleukin-1β Drives Disease Progression in Arrhythmogenic Cardiomyopathy.bioRxiv : the preprint server for biology · 2024Article
- Atrial fibrillation in cancer, anticancer therapies, and underlying mechanisms.Journal of molecular and cellular cardiology · 2024Review
- The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Myofibroblasts impair myocardial impulse propagation by heterocellular connexin43 gap-junctional coupling through micropores.Frontiers in physiology · 2024Article
- Fibroblasts, myofibroblasts and cardiac arrhythmias.The journal of cardiovascular aging · 2023Article
- Fir(e)ing the Rhythm: Inflammatory Cytokines and Cardiac Arrhythmias.JACC. Basic to translational science · 2023Review
- Cardiac Macrophages and Their Effects on Arrhythmogenesis.Frontiers in physiology · 2022Review
- Wide QRS-T angles are associated with markers of increased inflammatory activity independently of hypertension and diabetes.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2020Article
- What Is the Role of the Inflammation in the Pathogenesis of Heart Failure?Current cardiology reports · 2020Review
- Human pluripotent stem cell-derived cardiac stromal cells and their applications in regenerative medicine.Stem cell research · 2020Review
- Systemic Inflammation Rapidly Induces Reversible Atrial Electrical Remodeling: The Role of Interleukin-6-Mediated Changes in Connexin Expression.Journal of the American Heart Association · 2019Article
- Emerging Arrhythmic Risk of Autoimmune and Inflammatory Cardiac Channelopathies.Journal of the American Heart Association · 2018Review
- Review
- A Review of Interleukin-1 in Heart Disease: Where Do We Stand Today?Cardiology and therapy · 2018Review
- Featured Article: TGF-β1 dominates extracellular matrix rigidity for inducing differentiation of human cardiac fibroblasts to myofibroblasts.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- Article
- Illuminating Myocyte-Fibroblast Homotypic and Heterotypic Gap Junction Dynamics Using Dynamic Clamp.Biophysical journal · 2016Article
- The crossroads of inflammation, fibrosis, and arrhythmia following myocardial infarction.Journal of molecular and cellular cardiology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Following myocardial infarction (MI) inflammatory responses transform cardiac fibroblasts to myofibroblasts, which in vitro studies show form heterocellular gap junctions with cardiac myocytes via Connexin43 (Cx43). The ability to form heterocellular junctions in the intact heart and the impact of these junctions on propagation is unclear. We used a canine model of MI and characterized the distribution and quantity of myofibroblasts in surviving epicardial cells [epicardial border zone (EBZ)]. We found a significant increase in myofibroblasts within the EBZ and no gap junction plaques between myofibroblasts and myocytes. Because myofibroblasts produce IL-1β, which downregulates Cx43, we asked whether myofibroblast proliferation causes loss of Cx43 near myofibroblast clusters. In vitro studies showed that IL-1β caused loss of Cx43 and reduced coupling. Western blot showed a significant increase of IL-1β in the EBZ, and immunohistochemistry showed a loss of Cx43 in regions of myofibroblasts in the intact heart. Additionally, dye studies in intact heart showed no coupling between myocytes and myofibroblasts. To quantify the effect of myofibroblasts on propagation we used a two-dimensional subcellular computer model of the EBZ, which showed that heterogeneities in myofibroblast density lead to conduction abnormalities. In conclusion, an increase of myofibroblasts in the infarcted heart causes heterogeneous Cx43 levels, possibly as a result of the release of IL-1β and decreased cell-cell communication, which leads to conduction abnormalities following MI.
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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.