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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。
Cardiac Ca2 + homeostasis is an important factor in the occurrence of atrial fibrillation. FK506 Binding Protein 12.6 Regulates RyR2 Abnormality Leads to Ca2 + Leakage. Overexpression of Ca2 + -ATPase in Sarcoplasmic Reticulum Ca2 + Channel and Down-regulation of L-type Calcium Current in Atrial Cells Induced Ca2 + homeostasis when phosphoprotein is overexpressed Mechanism of atrial calcium control of some of the key sites may be the target of AF treatment. Atrial Ca2 + homeostasis by calcium release channels, SERCA2a, L-type calcium channel regulation, now the molecular mechanism of the current occurrence of atrial fibrillation were reviewed.