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缝隙连接是相邻心肌细胞间电、化学偶联的通道,亦是心室肌成为功能性合胞体的重要结构。心肌有缝隙连接蛋白(connexin,CX)40、43与45的表达,心室肌主要表达CX43。CX43形成的缝隙连接大部分呈点状分布于闰盘部位,心肌细胞膜侧面分布极少。心肌缺血-再灌注、肥厚、衰竭、高胆固醇与糖尿病条件下,心肌细胞缝隙连接均发生重塑。由以上疾病引起的重塑特征相似,均为CX43表达降低合并非均匀化、侧面化与去磷酸化。研究显示,这些重塑变化与心肌局部血管紧张素II浓度升高有关。缝隙连接CX43表达降低合并非均匀化改变电传导的各向异性,降低电传导速率。缝隙连接CX43的去磷酸化,不仅减慢缝隙连接电传导速度,而且降低其通透性。而侧面化的缝隙连接,可能使CX43形成的半通道增多,导致ATP外流与Na+内流,引起延迟后去极化。心肌病理条件下CX43的这些重塑,构成心律失常的基础。本文就心肌细胞缝隙连接重塑与心律失常的关系研究进展作一综述。
Gap junctions are channels of electrical and chemical coupling between adjacent cardiomyocytes, and are important structures of ventricular muscles that become functional syncytia. Cardiac muscle with connexin (CX) 40, 43 and 45 expression, the main expression of ventricular myocardium CX43. Most of the gap junctions formed by CX43 were distributed in spots on the intercalated disc, and there were very few lateral distribution of myocardial cell membrane. Myocardial ischemia - reperfusion, hypertrophy, failure, high cholesterol and diabetes, myocardial cell gap junctions are remodeled. The characteristics of the remodeling caused by the above diseases are similar, with reduced CX43 expression combined with nonhomogeneity, flanking and dephosphorylation. Studies have shown that these remodeling changes associated with elevated myocardial angiotensin II concentrations. Gap junctions CX43 expression Reduced combined heterogeneity alters the anisotropy of electrical conduction and decreases the rate of electrical conduction. The dephosphorylation of the gap junction CX43 not only slows the electrical conduction of the gap junction but also decreases its permeability. The flanking gap junction may increase the number of hemi-channels formed by CX43, resulting in ATP efflux and Na + influx, resulting in delayed depolarization. These remodeling of CX43 under cardiomyopathic conditions forms the basis of arrhythmia. This review summarizes the research progress of the relationship between cardiomyocyte gap junction remodeling and arrhythmia.