ArticleJournal of the American College of Cardiology2014
c-Src kinase inhibition reduces arrhythmia inducibility and connexin43 dysregulation after myocardial infarction.
Article in Journal of the American College of Cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 55 citations in OpenAlex.
- Hydrogen peroxide reduces Cx40, Cx43, and Cx45 gap junction function.Cell and tissue research · 2026Article
- Connexin 43 in Pathophysiology of Cardiac Diseases: From Molecular Mechanisms to Therapeutic Strategies.Physiological research · 2025Review
- Lysosomal CaCirculation. Arrhythmia and electrophysiology · 2025Article
- Cx45 regulation by kinases and impact of expression in heart failure.Journal of molecular and cellular cardiology · 2025Article
- Inhibition of Putative Ibrutinib Targets Promotes Atrial Fibrillation, Conduction Blocks, and Proarrhythmic Electrocardiogram Indices: A Mendelian Randomization Analysis.Cancer innovation · 2025Article
- c-Src Is Responsible for Mitochondria-Mediated Arrhythmic Risk in Ischemic Cardiomyopathy.Circulation. Arrhythmia and electrophysiology · 2024Article
- A Comprehensive Review of Cancer Drug-Induced Cardiotoxicity in Blood Cancer Patients: Current Perspectives and Therapeutic Strategies.Current treatment options in oncology · 2024Review
- Cardiac-specific deletion of BRG1 ameliorates ventricular arrhythmia in mice with myocardial infarction.Acta pharmacologica Sinica · 2024Article
- Evaluation of Tyrosine Kinase Inhibitors Loaded Injectable Hydrogels for Improving Connexin43 Gap Junction Intercellular Communication.ACS applied materials & interfaces · 2024Article
- Activation of Src Kinase Mediates the Disruption of Adherens Junction in the Blood-labyrinth Barrier after Acoustic Trauma.Current neurovascular research · 2024Article
- Inhibition of Pyk2 Improves Cx43 Intercalated Disc Localization, Infarct Size, and Cardiac Function in Rats With Heart Failure.Circulation. Heart failure · 2023Article
- Lysosomal CaPNAS nexus · 2023Article
- TRPM7 kinase mediates hypomagnesemia-induced seizure-related death.Scientific reports · 2023Article
- Dasatinib targets c-Src kinase in cardiotoxicity.Toxicology reports · 2023Article
- Off-Target Effects of Cancer Therapy on Development of Therapy-Induced Arrhythmia: A Review.Cardiology · 2023Review
- Article
- Hypoglycemia-Exacerbated Mitochondrial Connexin 43 Accumulation Aggravates Cardiac Dysfunction in Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Target Characterization of Kaempferol against Myocardial Infarction Using Novel In Silico Docking and DARTS Prediction Strategy.International journal of molecular sciences · 2021Article
- Serine-threonine protein phosphatase regulation of Cx43 dephosphorylation in arrhythmogenic disorders.Cellular signalling · 2021Review
- Inhibition of the unfolded protein response reduces arrhythmia risk after myocardial infarction.The Journal of clinical investigation · 2021Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
objectivesThe aim of this study was to evaluate the role of tyrosine kinase cellular-Src (c-Src) inhibition on connexin43 (Cx43) regulation in a mouse model of myocardial infarction (MI).
backgroundMI is associated with decreased expression of Cx43, the principal gap junction protein responsible for propagating current in ventricles. Activated c-Src has been linked to Cx43 dysregulation.
methodsMI was induced in 12-week-old mice by coronary artery occlusion. MI mice were treated with c-Src inhibitors (PP1 or AZD0530), PP3 (an inactive analogue of PP1), or saline. Treated hearts were compared to sham mice by echocardiography, optical mapping, telemetry electrocardiographic monitoring, and inducibility studies. Tissues were collected for immunoblotting, quantitative polymerase chain reaction, and immunohistochemistry.
resultsActive c-Src was elevated in PP3-treated MI mice compared to sham at the scar border (280%, p = 0.003) and distal ventricle (346%, p = 0.013). PP1 treatment restored active c-Src to sham levels at the scar border (86%, p = 0.95) and distal ventricle (94%, p = 1.0). PP1 raised Cx43 expression by 69% in the scar border (p = 0.048) and by 73% in the distal ventricle (p = 0.043) compared with PP3 mice. PP1-treated mice had restored conduction velocity at the scar border (PP3: 32 cm/s, PP1: 41 cm/s, p < 0.05) and lower arrhythmic inducibility (PP3: 71%, PP1: 35%, p < 0.05) than PP3 mice. PP1 did not change infarct size, electrocardiographic pattern, or cardiac function. AZD0530 treatment demonstrated restoration of Cx43 comparable to PP1.
conclusionsc-Src inhibition improved Cx43 levels and conduction velocity and lowered arrhythmia inducibility after MI, suggesting a new approach for arrhythmia reduction following MI.
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