ArticleAnatolian journal of cardiology2017
Connexin 43 is involved in the sympathetic atrial fibrillation in canine and canine atrial myocytes.
Article in Anatolian journal of cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Association BetweenFrontiers in cardiovascular medicine · 2020Pooled it
- Trends in Chronic Ischemic Heart Disease-Related Mortality in Older Adults With Atrial Fibrillation (1999-2023): A CDC WONDER Database Analysis.Clinical cardiology · 2026Article
- Sex Differences in the Expression of Cardiac Remodeling and Inflammatory Cytokines in Patients with Obstructive Sleep Apnea and Atrial Fibrillation.Biomedicines · 2024Article
- Atrial Fibrillation and Chronic Coronary Ischemia: A Challenging Vicious Circle.Life (Basel, Switzerland) · 2023Review
- Liposome-Encapsulated Hemoglobin Vesicle Improves Persistent Anti-arrhythmogenesis through Improving Myocardial Electrical Remodeling and Modulating Cardiac Autonomic Activity in a Hemorrhagic Shock-Induced Rat Heart Model.Current medical science · 2023Article
- Article
- Enhanced atrial internal-external neural remodeling facilitates atrial fibrillation in the chronic obstructive sleep apnea model.PloS one · 2021Article
- Article
- Cardiac Sympathetic Denervation Suppresses Atrial Fibrillation and Blood Pressure in a Chronic Intermittent Hypoxia Rat Model of Obstructive Sleep Apnea.Journal of the American Heart Association · 2019Article
- Time Series Gene Expression Profiling and Temporal Regulatory Pathway Analysis of Angiotensin II Induced Atrial Fibrillation in Mice.Frontiers in physiology · 2019Article
- Connexins and Atrial Fibrillation in Obstructive Sleep Apnea.Current sleep medicine reports · 2018Article
- Activin Receptor-Like Kinase 4 Haplodeficiency Mitigates Arrhythmogenic Atrial Remodeling and Vulnerability to Atrial Fibrillation in Cardiac Pathological Hypertrophy.Journal of the American Heart Association · 2018Article
- Cardiac Arrhythmias and Antiarrhythmic Drugs: An Autophagic Perspective.Frontiers in physiology · 2018Article
- Regeneration of glycocalyx by heparan sulfate and sphingosine 1-phosphate restores inter-endothelial communication.PloS one · 2017Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAtrial fibrillation (AF) is the most common rapid cardiac arrhythmia associated with high morbidity and mortality. Stimulation of the sympathetic nerve is involved in AF occurrence. The gap junction protein connexin 43 (Cx43) plays a key role in electrical conduction velocity in cardiac tissues, and under expression of Cx43 was linked with AF. The aim of this study was to investigate whether Cx43 was involved in sympathetic AF.
methodsFifteen dogs were randomly divided into 3 groups (5 in each group). Sympathetic AF was induced in dogs and isolated canine atrial myocytes by isoproterenol (ISO) perfusion and rapid atrium pacing (RAP). The expression levels of nerve growth factor (NGF) and tyrosine hydroxylase (TH) in the atrial tissues were detected using immunohistochemical staining. The transcription and protein expression of Cx43 in the AF cell model was measured. Subsequently, Cx43 was blocked by short interfering (si) RNA in atrial myocytes and the gap junctional intercellular communication was detected using the scrape-loading and dye transfer assay.
resultsSympathetic AF was successfully induced by a combination of ISO perfusion and RAP. The expression levels of NGF and TH were increased in the RAP group, and further increased in the RAP + ISO group. Tissue samples from the AF dogs had a lower Cx43 level than those of the control group (p<0.05). The expressions of mRNA and protein of Cx43 in sympathetic AF cell model decreased by 26% and 28%, respectively, when compared with the control group, with p<0.05. Silencing Cx43 in cells by siRNA could also efficiently reduce Cx43 expression. The relative levels of Cx45 mRNA were decreased by 73% compared with unaffected cells. The scrape-loading and dye transfer assay showed that gap junctional intercellular communication was hampered in the sympathetic AF cell model and silencing Cx43 could impede channel conduction.
conclusionThe results suggested that low expression of Cx43 was involved in sympathetic AF by influencing intercellular channel conduction. Intervention of Cx43 expression might be an appealing therapy to sympathetic AF.
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