心肌细胞兴奋-收缩偶联的微观机制

心肌细胞的兴奋 收缩偶联 (ECC)本质上是胞膜上的电压门控L 型钙通道 (LCCs)和胞内ryanodine受体 (RyRs)之间通过钙诱导钙释放 (CICR)机制进行沟通进而引发肌细胞收缩的过程。最近的研究进一步揭示了微观水平上LCCs和RyRs之间的信息联系。在钙偶联位点 (couplons)上 ,LCCs因膜去极化而随机开放 ,在局部产生高强度的钙脉冲 (即钙小星 ,Ca2 sparklet) ,作用于邻近肌质网终末池上的RyRs。钙偶联位点通过由钙小星随机激活的RyRs(即钙释放通道 )以钙火花 (Ca2 spark)的形式释放钙。这些钙在全细胞水平上总和即形成钙瞬变 (Ca2 transient)。因此 ,钙小星触发钙火花就构成了ECC中的基本事件。本文重点阐述LCCs和RyRs分子间的信号转导机制 ,也即从微观水平上探讨CICR及ECC的形成机制。

Microscopic mechanism of excitation-contraction coupling in cardiac myocytes

Cardiac excitation-contraction coupling (ECC) is, in es se nce, a communication process between sarcolemmal voltage-dependent L-type calc ium channels (LCCs) and ryanodine receptors (RyRs) of sarcoplasmic reticulum (SR ) by the mechanism of calcium-induced calcium release (CICR). Recent advances d isplayed more information about the microscopic signaling between LCCs and RyRs. In calcium release couplons, the calcium influx through the opening of LCCs by membrane depolarization forms calcium sparklets locally which then act on the ad jacent SR RyRs. Stochastic activation of RyRs discharges calcium sparks from dif ferent calcium couplons, which summate into global calcium transients. Therefore , ignition of calcium sparks by calcium sparklets constitutes the elementary eve nts in ECC. This review focuses on the intermolecular signaling between LCCs and RyRs, to describe the microscopic view of CICR and ECC.