摘要
心肌细胞内Ca2+稳态异常是心房颤动发生的重要因素。FK506结合蛋白12.6调控RyR2的异常导致Ca2+漏出,受磷蛋白表达过高时对肌质网钙摄取通道Ca2+ATP酶的过度调控以及心房细胞L型钙电流的下调都是导致心房Ca2+稳态异常的机制,心房钙调控的一些关键部位则可能成为房颤治疗的靶点。心房内Ca2+稳态受钙释放通道、SERCA2a、L型钙通道等的调控,现就目前房颤发生机制的分子机制予以综述。
The disrupted cardiomyocytic Ca^2＋ homeostasis is a major cause of atrial fibrillation.The dysregulation of RyR2 by FK506 binding protein 12.6 leads to the leakage of Ca^2＋.The overexpression of phospholamban that causes the overregulation of sarcoplasmic calcium uptake channel Ca^2＋-ATPase and the downregulation of atrial cardiomyocytic L-type calcium current are thought to be the mechanisms of disrupted atrial Ca^2＋ homeostasis.Some key links of atrial calcium regulation may be potential therapeutic targets for atrial fibrillation.The atrial Ca^2＋ homeostasis is regulated by calcium release channel,SERCA2a,and L-type calcium channel.This article reviews the molecular mechanisms of atrial fibrillation.
出处
《医学综述》
2011年第4期484-486,共3页
Medical Recapitulate
基金
国家自然科学基金(81070140)
关键词
心房颤动
钙稳态
分子机制
Atrial fibrillation
Ca2＋ homeostasis
Molecular mechanisms
