ArticleCardiovascular research2009
Cx43 CT domain influences infarct size and susceptibility to ventricular tachyarrhythmias in acute myocardial infarction.
Article in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- Viral Infection and Connexin Dysfunction in the Heart.Current cardiology reports · 2025Review
- Inhibition of Gap Junction Formation Prior to Implantation of Bone Marrow-Derived Mesenchymal Cells Improves Function in the Ischemic Myocardium.International journal of molecular sciences · 2023Article
- GJA1-20k and Mitochondrial Dynamics.Frontiers in physiology · 2022Review
- Cx43 carboxyl terminal domain determines AQP4 and Cx30 endfoot organization and blood brain barrier permeability.Scientific reports · 2021Article
- Impaired Cx43 gap junction endocytosis causes morphological and functional defects in zebrafish.Molecular biology of the cell · 2021Article
- Connexins in the Heart: Regulation, Function and Involvement in Cardiac Disease.International journal of molecular sciences · 2021Review
- Uric acid preconditioning alleviated doxorubicin induced JNK activation and Cx43 phosphorylation associated cardiotoxicity via activation of AMPK-SHP2 signaling pathway.Annals of translational medicine · 2020Article
- Inhibition of MicroRNA-206 Ameliorates Ischemia-Reperfusion Arrhythmia in a Mouse Model by Targeting Connexin43.Journal of cardiovascular translational research · 2020Article
- Stress response protein GJA1-20k promotes mitochondrial biogenesis, metabolic quiescence, and cardioprotection against ischemia/reperfusion injury.JCI insight · 2018Article
- Connexins and Disease.Cold Spring Harbor perspectives in biology · 2018Review
- Simulated microgravity hampers Notch signaling in the fight against myocardial ischemia‑reperfusion injury.Molecular medicine reports · 2018Article
- Comparative regenerative mechanisms across different mammalian tissues.NPJ Regenerative medicine · 2018Review
- Cysteine residues in the cytoplasmic carboxy terminus of connexins dictate gap junction plaque stability.Molecular biology of the cell · 2017Article
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
- Dedifferentiation, Proliferation, and Redifferentiation of Adult Mammalian Cardiomyocytes After Ischemic Injury.Circulation · 2017Article
- Defective signaling, osteoblastogenesis and bone remodeling in a mouse model of connexin 43 C-terminal truncation.Journal of cell science · 2017Article
- Electrophysiological alterations in a murine model of chronic coxsackievirus B3 myocarditis.PloS one · 2017Article
- A 14-3-3 mode-1 binding motif initiates gap junction internalization during acute cardiac ischemia.Traffic (Copenhagen, Denmark) · 2014Article
- c-Src kinase inhibition reduces arrhythmia inducibility and connexin43 dysregulation after myocardial infarction.Journal of the American College of Cardiology · 2014Article
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4 authors at 3 institutions in 1 country.
Funding
Abstract
aimsHearts of mice expressing K258stop in place of connexin43 (Cx43) protein were subjected to acute myocardial infarction in order to assess the importance of Cx43 regulation on infarct size and arrhythmia susceptibility. This mutation K258stop prevents chemical regulation of Cx43 channels, including by low intracellular pH. METHODS AND
resultsLangendorff-perfused hearts of mice harbouring one Cx43 knockout (KO) allele and one K258stop or Cx43 allele (K258stop/KO; Cx43/KO as control) were subjected to 1 h of ischaemia and 4 h of reperfusion by reversibly occluding the left anterior descending (LAD) coronary artery. Inducibility of ventricular tachyarrhythmias (VTs) was tested by applying an endocardial burst-pacing protocol during LAD occlusion. Separately, time course and the extent of acidification-induced closure of gap junction channels were tested by dual-voltage clamp. Infarct volume (as per cent of area at risk) was significantly larger in K258stop/KO hearts compared with Cx43/KO controls (42.2 +/- 3 vs. 30.4 +/- 1.7%, P = 0.004, n = 8 each). During LAD occlusion, K258stop/KO hearts had a higher incidence of pacing-induced VT and a higher frequency of occurrence of spontaneous premature ventricular beats. The occurrence of ventricular arrhythmias was also significantly larger in the K258stop/KO hearts during reperfusion. In separate experiments, we demonstrated reduced sensitivity to acidification-induced uncoupling in cell pairs obtained from K258stop/KO hearts.
conclusionLoss of the regulatory domain of Cx43 leads to an increase in infarct size and increased susceptibility to arrhythmias following acute coronary occlusion.
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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.