T-type calcium channel expression and function in the diseased heart
T-type calcium channel expression and function in the diseased heart
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DOI：
10.4161/chan.4.6.12870
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发表时间：
2010-11-01
期刊：
影响因子：
3.3
通讯作者：
Cribbs, Leanne L.
中科院分区：
文献类型：
--
作者：
Cribbs, Leanne L.
细胞内Ca2+的调节对心肌细胞功能至关重要，调节Ca2+内流的蛋白质的改变对患病心脏有可怕的后果。低电压激活的t型Ca2+通道是Ca2+进入的一种途径，根据成人心脏的发育阶段和病理条件进行调节。心脏t型通道主要包括Ca(V)3.1 （α 1G）和Ca(V)3.2 （α 1H）两种类型，在疾病和损伤时均可在心肌中诱导，但对其调控机制和各自功能的了解相对较少。本文整合了之前的数据，建立了心脏疾病动物模型中t型Ca2+通道的调节，以及最近的数据，开始解决心脏Ca(V)3.1和Ca(V)3.2 Ca2+通道在病理环境中的表达的功能后果。在心肌肥厚的背景下，t型Ca2+通道与Ca2+依赖性信号通路的推定关联也进行了讨论。
The regulation of intracellular Ca2+ is essential for cardiomyocyte function, and alterations in proteins that regulate Ca2+ influx have dire consequences in the diseased heart. Low voltage activated, T-type Ca2+ channels are one pathway of Ca2+ entry that is regulated according to developmental stage and in pathological conditions in the adult heart. Cardiac T-type channels consist of two main types, Ca(V)3.1 (alpha 1G) and Ca(V)3.2 (alpha 1H), and both can be induced in the myocardium in disease and injury but still, relatively little is known about mechanisms for their regulation and their respective functions. This article integrates previous data establishing regulation of T-type Ca2+ channels in animal models of cardiac disease, with recent data that begin to address the functional consequences of cardiac Ca(V)3.1 and Ca(V)3.2 Ca2+ channel expression in the pathological setting. The putative association of T-type Ca2+ channels with Ca2+ dependent signaling pathways in the context of cardiac hypertrophy is also discussed.