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Voltage-Gated Calcium Channels in Nonexcitable Tissues
Annual Review of Physiology ( IF 18.2 ) Pub Date : 2021-02-10 , DOI: 10.1146/annurev-physiol-031620-091043
Geoffrey S Pitt 1 , Maiko Matsui 1 , Chike Cao 1
Affiliation  

The identification of a gain-of-function mutation in CACNA1C as the cause of Timothy syndrome, a rare disorder characterized by cardiac arrhythmias and syndactyly, highlighted roles for the L-type voltage-gated Ca2+ channel CaV1.2 in nonexcitable cells. Previous studies in cells and animal models had suggested that several voltage-gated Ca2+ channels (VGCCs) regulated critical signaling events in various cell types that are not expected to support action potentials, but definitive data were lacking. VGCCs occupy a special position among ion channels, uniquely able to translate membrane excitability into the cytoplasmic Ca2+ changes that underlie the cellular responses to electrical activity. Yet how these channels function in cells not firing action potentials and what the consequences of their actions are in nonexcitable cells remain critical questions. The development of new animal and cellular models and the emergence of large data sets and unbiased genome screens have added to our understanding of the unanticipated roles for VGCCs in nonexcitable cells. Here, we review current knowledge of VGCC regulation and function in nonexcitable tissues and cells, with the goal of providing a platform for continued investigation.

中文翻译:


非兴奋性组织中的电压门控钙通道

鉴定CACNA1C中的功能获得性突变是 Timothy 综合征(一种以心律失常和并指症为特征的罕见疾病)的原因,突出了 L 型电压门控 Ca 2+通道 Ca V 1.2 在不可兴奋细胞中的作用。先前对细胞和动物模型的研究表明,几种电压门控 Ca 2+通道 (VGCC) 调节各种细胞类型中的关键信号事件,这些事件预计不会支持动作电位,但缺乏确定的数据。VGCC 在离子通道中占据特殊位置,能够独特地将膜兴奋性转化为细胞质 Ca 2+细胞对电活动反应的变化。然而,这些通道如何在不激发动作电位的细胞中发挥作用,以及它们的作用在不可兴奋细胞中的后果如何,仍然是关键问题。新动物和细胞模型的发展以及大数据集和无偏见基因组筛选的出现增加了我们对 VGCC 在不可兴奋细胞中的意外作用的理解。在这里,我们回顾了当前关于 VGCC 在非兴奋性组织和细胞中的调节和功能的知识,目的是为继续研究提供一个平台。

更新日期:2021-02-11
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