Wingertzahn M A, Ochs R S
Department of Pharmacy and Allied Health, St. Johns University, Jamaica, New York, USA.
Mol Genet Metab. 1998 Oct;65(2):113-20. doi: 10.1006/mgme.1998.2746.
The missing link in our understanding of excitation-contraction coupling (ECC) in skeletal muscle is the mechanism by which Ca2+ increases in the cytosol to trigger contraction. We discuss here a general background of intracellular Ca2+ handling, some characteristics of the major proteins involved in Ca2+ flow during ECC, and mechanisms currently believed to explain the increase in Ca2+ upon stimulation of muscle cells. These mechanisms include the calcium-induced calcium release, the direct coupled mechanism in which a plasma membrane and sarcoplasmic reticulum membrane protein interact, and mechanisms involving Ca2+ secretagogues that are known to elicit increases in calcium in other cells, inositol trisphosphate, and cyclic ADP ribose. We also consider possible roles for proteins associated with the principal calcium release channel of the sarcoplasmic reticulum, the ryanodine receptor. Finally, we discuss malignant hyperthermia, a disease associated directly with aberrant control of muscle cell calcium release.
我们对骨骼肌兴奋-收缩偶联（ECC）理解中的缺失环节是胞质溶胶中Ca2+增加以触发收缩的机制。我们在此讨论细胞内Ca2+处理的一般背景、ECC期间参与Ca2+流动的主要蛋白质的一些特性，以及目前认为可解释肌肉细胞受刺激后Ca2+增加的机制。这些机制包括钙诱导的钙释放、质膜和肌浆网膜蛋白相互作用的直接偶联机制，以及涉及已知可引起其他细胞钙增加的Ca2+促分泌剂、肌醇三磷酸和环ADP核糖的机制。我们还考虑了与肌浆网主要钙释放通道——兰尼碱受体相关的蛋白质的可能作用。最后，我们讨论恶性高热，一种与肌肉细胞钙释放的异常控制直接相关的疾病。
