ArticleScientific reports2018
Overexpression of Cx43 in cells of the myocardial scar: Correction of post-infarct arrhythmias through heterotypic cell-cell coupling.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The trial behind it
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Interstitial cells and arrhythmia.American journal of physiology. Cell physiology · 2026Review
- Connexin-43 Restoration Alleviates Desmosomal Arrhythmogenic Cardiomyopathy.Circulation. Heart failure · 2026Article
- Efficient in vivo targeting of the myocardial scar using Moloney murine leukaemia virus complexed with nanoparticles.The Journal of physiology · 2026Article
- Models of cardiomyocyte-non-myocyte electrical interactions.The Journal of physiology · 2026Review
- Gap junctional and ephaptic coupling in cardiac electrical propagation: homocellular and heterocellular perspectives.The Journal of physiology · 2026Review
- A Redox-Active and Electroactive Hydrogel Enabled by an Integrated PEDOT@PMOF Nanofiller for Post-Infarct Myocardial Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Overexpression of Cx43: Is It an Effective Approach for the Treatment of Cardiovascular Diseases?Biomolecules · 2025Review
- Nanoparticle-assisted targeting of heart lesions with cardiac myofibroblasts: Combined gene and cell therapy.Theranostics · 2025Article
- CCRR regulate MYZAP-PKP2-Nav1.5 signaling pathway in atrial fibrillation following myocardial infarction.iScience · 2024Article
- Implications for neutrophils in cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2024Review
- Myofibroblasts impair myocardial impulse propagation by heterocellular connexin43 gap-junctional coupling through micropores.Frontiers in physiology · 2024Article
- 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
- Combination human umbilical cord perivascular and endothelial colony forming cell therapy for ischemic cardiac injury.NPJ Regenerative medicine · 2023Article
- Distinct Cardiac Connexin-43 Expression in Hypertrophied and Atrophied Myocardium May Impact the Vulnerability of the Heart to Malignant Arrhythmias. A Pilot Study.Physiological research · 2023Article
- Identification of Cx43 variants predisposing to ventricular fibrillation in the acute phase of ST-elevation myocardial infarction.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 · 2023Article
- Cardiac Piezo1 Exacerbates Lethal Ventricular Arrhythmogenesis by Linking Mechanical Stress with CaResearch (Washington, D.C.) · 2023Article
- Protective Effects of Therapeutic Neutrophil Depletion and Myeloperoxidase Inhibition on Left Ventricular Function and Remodeling in Myocardial Infarction.Antioxidants (Basel, Switzerland) · 2022Article
- Apelin-13 Increases Functional Connexin-43 through Autophagy Inhibition via AKT/mTOR Pathway in the Non-Myocytic Cell Population of the Heart.International journal of molecular sciences · 2022Article
- Glycogen synthase kinase 3 beta inhibitor SB216763 improves Kir2.1 expression after myocardia infraction in rats.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2022Article
Corrections and comments
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Authors and funding
24 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ventricular tachycardia (VT) is the most common and potentially lethal complication following myocardial infarction (MI). Biological correction of the conduction inhomogeneity that underlies re-entry could be a major advance in infarction therapy. As minimal increases in conduction of infarcted tissue markedly influence VT susceptibility, we reasoned that enhanced propagation of the electrical signal between non-excitable cells within a resolving infarct might comprise a simple means to decrease post-infarction arrhythmia risk. We therefore tested lentivirus-mediated delivery of the gap-junction protein Connexin 43 (Cx43) into acute myocardial lesions. Cx43 was expressed in (myo)fibroblasts and CD45
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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.