论文部分内容阅读
心肌细胞 L 型钙电流 ( IC a· L)触发了 Ca2 +诱导的 Ca2 +释放 ( CICR) ,调节着细胞内瞬时 Ca2 +动力学 ,从而在兴奋—收缩耦联过程中起关键性作用。ICa· L密度和通道功能的改变参与了心力衰竭的发生。作者综述了 :1L型 Ca2 +通道的结构和生理作用 ;2肥大和衰竭的心肌 ICa· L变化及其频率依赖性调节机制 ;3 Ca2 + 通道和心力衰竭的治疗关系 ;4L型 Ca2 +通道未来研究方向
L-type calcium currents in cardiomyocytes (ICa · L) trigger Ca2 + -induced Ca2 + release (CICR), regulating intracellular transient Ca2 + dynamics and thereby playing a pivotal role in excitatory-contractile coupling. Changes in ICa · L density and channel function are involved in the development of heart failure. The authors summarize the structural and physiological roles of 1L-type Ca2 + channels, 2 changes in ICa-L and its frequency-dependent regulation of hypertrophic and failing myocardium, 3 the therapeutic relationship between Ca2 + channels and heart failure, 4L Ca2 + channels in the future research direction