Calcium Signaling in Cardiac Myocytes
Calcium Signaling in Cardiac Myocytes
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DOI：
10.1101/cshperspect.a004242
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发表时间：
2011-11-01
影响因子：
7.2
通讯作者：
Bootman, Martin D.
中科院分区：
文献类型：
--
作者：
Fearnley, Claire J.;Roderick, H. Llewelyn;Bootman, Martin D.
钙(Ca~(2+))是心肌细胞功能的重要调节因子。主要是，钙离子是贯穿心脏的电信号和推动血液的心肌细胞收缩之间的纽带。此外，钙离子还控制着许多其他心肌细胞的活动，包括基因转录。心肌钙信号转导主要依赖于一些关键的分子分子--兰尼定受体、电压控制的钙通道和钙泵/转运体。这些部分负责在细胞去极化时产生钙信号，在细胞收缩后恢复钙信号，并设定基础条件。虽然这些是心脏钙离子流动的中心角色，但信号机制和辅助蛋白网络对心脏钙信号进行复杂的调节。心脏钙信号机制组件的细微变化，即使是通过突变、疾病或血流动力学需求的慢性改变，也可能对心肌细胞的功能和表型产生深远的影响。在这里，我们讨论了在心室和心房肌细胞中潜在的钙信号转导机制。特别是，我们描述了参与钙信号产生和逆转的关键参与者的作用和调节。
Calcium (Ca2+) is a critical regulator of cardiac myocyte function. Principally, Ca2+ is the link between the electrical signals that pervade the heart and contraction of the myocytes to propel blood. In addition, Ca2+ controls numerous other myocyte activities, including gene transcription. Cardiac Ca2+ signaling essentially relies on a few critical molecular players-ryanodine receptors, voltage-operated Ca2+ channels, and Ca2+ pumps/transporters. These moieties are responsible for generating Ca2+ signals upon cellular depolarization, recovery of Ca2+ signals following cellular contraction, and setting basal conditions. Whereas these are the central players underlying cardiac Ca2+ fluxes, networks of signaling mechanisms and accessory proteins impart complex regulation on cardiac Ca2+ signals. Subtle changes in components of the cardiac Ca2+ signaling machinery, albeit through mutation, disease, or chronic alteration of hemodynamic demand, can have profound consequences for the function and phenotype of myocytes. Here, we discuss mechanisms underlying Ca2+ signaling in ventricular and atrial myocytes. In particular, we describe the roles and regulation of key participants involved in Ca2+ signal generation and reversal.