Regulation of sarcoplasmic reticulum calcium release by luminal calcium in cardiac muscle.
Regulation of sarcoplasmic reticulum calcium release by luminal calcium in cardiac muscle.
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DOI：
10.1007/0-387-23188-9_7
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发表时间：
2002-06
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影响因子：
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通讯作者：
S. Györke;I. Györke;V. Lukyanenko;D. Terentyev;S. Viatchenko‐Karpinski;T. Wiesner
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文献类型：
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作者：
S. Györke;I. Györke;V. Lukyanenko;D. Terentyev;S. Viatchenko‐Karpinski;T. Wiesner
心肌兴奋-收缩偶联依赖于肌浆网（SR）的瞬时流出，SR是肌肉细胞内的储存和释放细胞器。虽然导致释放开始的事件已经得到了很好的确立，并且已知涉及SR释放通道/ryanodine受体（RyR 2）的激活，其从细胞外环境进入细胞溶质（即释放，CICR），63，200负责SR释放终止的机制仅开始出现。然而，这些约束机制是特别重要的，鉴于固有的倾向，CICR的自我激活。由于释放到胞质溶胶中具有反馈释放通道以诱导更多释放的趋势，因此预期存在某种负控制机制，其解释了心肌细胞中CICR的终止。越来越多的证据表明，抑制和终止CICR涉及SR腔内的信号传导过程。201特别地，释放期间游离SR内浓度的下降提供了RyR 2闭合（即管腔失活）的信号，202导致CICR的稳健终止和持续直到SR恢复的不应状态。最近，SR管腔内结合蛋白钙螯合蛋白（CASQ 2）的遗传缺陷与遗传性心律失常有关，
Cardiac excitation-contraction (EC) coupling relies on transient efflux of from the sarcoplamic reticulum (SR), an intracellular storage and release organelle in muscle. While the events leading to initiation of release have been well established and are known to involve activation of the SR release channels/ryanodine receptors (RyR2s) by that enters the cytosol from the extracellular milieu (ie release, CICR), 63,200 the mechanisms responsible for SR release termination only begin to emerge. Yet, these restraining mechanisms are of particular importance in view of the inherent predisposition of CICR to self-activation. Because released to the cytosol has the tendency to feedback on the release channels to induce more release, it is expected that some sort of negative control mechanisms exist that account for termination of CICR in cardiac mytocytes. Growing evidence indicates that restraining and termination of CICR involves signaling processes inside the SR lumen. 201 In particular, the decline of free intra-SR concentration during release provides a signal for RyR2 closure (ie luminal deactivation), 202 resulting in robust termination of CICR and in a refractory state that lasts till is restored by the SR Recently, genetic defects in the SR intraluminal binding protein calsequestrin (CASQ2) have been linked to inherited cardiac arrhythmia and