Calcium entry in skeletal muscle.
Calcium entry in skeletal muscle.
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骨骼肌中的钙进入。
DOI：
10.1113/jphysiol.2009.172585
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发表时间：
2009
期刊：
影响因子：
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通讯作者：
Rosenberg,PaulB
中科院分区：
文献类型：
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作者：
Rosenberg,PaulB
几十年前就已经确定，兴奋-收缩（EC）耦合依赖于骨骼肌收缩时储存的钙的去极化依赖性释放，从那时起，许多研究小组进行了大量的努力，详细阐述了EC耦合背后钙释放的分子机制（Edman & Grieve, 1964; Caputo & Gimenez, 1967; Luttgau & Oetliker, 1968）。最近，越来越多的证据表明，骨骼肌中存在依赖钙进入的替代钙信号通路（Hopf etal . 1996; Kurebayashi & Ogawa, 2001）。在这次研讨会上，RT Dirksen提供了骨骼肌钙进入的重要概述（Dirksen, 2009）。骨骼肌纤维中的钙离子进入有两种形式：兴奋耦合钙进入（ECCE）和储存操作钙进入（SOCE）（Williams & Rosenberg, 2002； Cherednichenko等人，2004）。肌细胞中的ECCE在膜去极化延长后被激活，这与钙储存无关。ECCE需要l型钙通道（LTCC）和ryanodine受体（RYR1）通道的功能，但该孔的分子身份尚未明确，尽管可能涉及LTCC （Hurne et al. 2005; Bannister et al. 2008, 2009）。恶性高热（MH）中ECCE发生改变，可能导致MH患者肌纤维中钙信号紊乱（Cherednichenko等人，2008年）。另一方面，SOCE需要消耗内部储存，并在不可兴奋细胞中得到最好的表征（Putney, 1986, 2007）。前段时间在肌管中描述了骨骼肌中的SOCE (Hopf etal . 1996)，但直到在不可兴奋细胞中发现两个重要分子基质相互作用分子1 （STIM1）和Orai1，才认识到SOCE的重要性
It was established decades ago that excitation–contraction (EC) coupling relies on the depolarization-dependent release of stored calcium for skeletal muscle contraction and since that time considerable effort by many groups have detailed the molecular mechanism of calcium release underlying EC coupling (Edman & Grieve, 1964; Caputo & Gimenez, 1967; Luttgau & Oetliker, 1968). More recently, growing evidence suggests that alternative calcium signalling pathways exist in skeletal muscles that rely on calcium entry (Hopf et al. 1996; Kurebayashi & Ogawa, 2001). In this symposium, RT Dirksen provided an important overview of calcium entry in skeletal muscle (Dirksen, 2009). Two forms of Ca2+ entry have been characterized in skeletal muscle fibres: excitation-coupled calcium entry (ECCE) and store-operated calcium entry (SOCE)(Williams & Rosenberg, 2002; Cherednichenko et al. 2004). ECCE is activated in muscle cells following prolonged membrane depolarization that is independent of the calcium stores. ECCE requires functioning L-type calcium channel (LTCC) and ryanodine receptor (RYR1) channels, but the molecular identity of the pore remains undefined although it is likely to involve the LTCC (Hurne et al. 2005; Bannister et al. 2008, 2009).ECCE is altered in malignant hyperthermia (MH) and may contribute to the disordered calcium signalling found in muscle fibres of MH patients (Cherednichenko et al. 2008). SOCE on the other hand requires depletion of the internal stores and has been best characterized in non-excitable cells (Putney, 1986, 2007). SOCE in skeletal muscle was described some time ago in myotubes (Hopf et al. 1996), but it was not until the discovery of two important molecules, stromal interaction molecule 1 (STIM1) and Orai1 in non-excitable cells, that the importance of