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Connexin43 and Myocardial Ischemia-Reperfusion Injury

连接蛋白 心肌缺血 再灌注损伤 医学 缺血 机制(生物学) 心肌病 心脏病学 缝隙连接 内科学 心力衰竭 化学 生物化学 细胞内 认识论 哲学
作者
Lingyun Zu,Ningxin Wen,Changjie Liu,Mingming Zhao,Lemin Zheng
出处
期刊:Cardiovascular and Hematological Disorders - Drug Targets [Bentham Science Publishers]
卷期号:18 (1): 14-16 被引量:12
标识
DOI:10.2174/1871529x16666161227143644
摘要

Background: Recently, the treatment and prevention of ischemic cardiomyopathy is one of the emerging research topics in the cardiovascular field. Gap junction is the basic structure of cardiac electrophysiology. Connexin is the basic unit of gap junctions. Connexin43(CX43) is the most abundant member of Cx family in the heart, the normal expression of Cx43 is important for heart development, electrically coupled cardiomyocytes activities and coordination of myocardial function. The connection between Cx43 and myocardial ischemia/reperfusion or reperfusion injury has become the focus of current research. Methods: We undertook a structured search of bibliographic database for peer-reviewed research literature using a focused review question and inclusion/exclusion criteria. The quality of retrieved papers was appraised using standard tools. The characteristics of screened papers were described, and a deductive qualitative content analysis methodology was applied to analyze the interventions and findings of included studies using a conceptual framework. Results: Twenty-one papers were included in the review, eight papers outlined the relationship of Cx43 and reperfusion arrhythmias. Eight papers pointed out the effect on the infarct size of Cx43. Conclusion: The findings of this review confirm that Cx43 is the most abundant member of Cx family in the heart and is vital for myocardial protection during ischemia/reperfusion process and for ischemia/reperfusion injury. Many of its mechanism are still not very clear and require future research in the future. Keywords: Gap junction, connexin 43, myocardial ischemia/reperfusion, electrophysiology, polypeptide, endothelial cells.

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