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Regulation of calcium channels in smooth muscle: New insights into the role of myosin light chain kinase

机译:平滑肌中钙通道的调节:肌球蛋白轻链激酶作用的新见解

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摘要

Smooth muscle myosin light chain kinase (MLCK) plays a crucial role in artery contraction, which regulates blood pressure and blood flow distribution. In addition to this role, MLCK contributes to Ca2+ flux regulation in vascular smooth muscle (VSM) and in non-muscle cells, where cytoskeleton has been suggested to help Ca2+ channels trafficking. This conclusion is based on the use of pharmacological inhibitors of MLCK and molecular and cellular techniques developed to down-regulate the enzyme. Dissimilarities have been observed between cells and whole tissues, as well as between large conductance and small resistance arteries. A differential expression in MLCK and ion channels (either voltage-dependent Ca2+ channels or non-selective cationic channels) could account for these observations, and is in line with the functional properties of the arteries. A potential involvement of MLCK in the pathways modulating Ca2+ entry in VSM is described in the present review.
机译:平滑肌肌球蛋白轻链激酶(MLCK)在动脉收缩中起着关键作用,它调节血压和血流分布。除此作用外,MLCK还有助于调节血管平滑肌(VSM)和非肌肉细胞中的Ca2 +通量,在这些细胞中,细胞骨架被认为有助于Ca2 +通道的运输。该结论是基于使用MLCK的药理抑制剂以及开发来下调该酶的分子和细胞技术。已经观察到细胞与整个组织之间以及大电导和小阻力动脉之间存在差异。 MLCK和离子通道(取决于电压的Ca2 +通道或非选择性阳离子通道)中的差异表达可以解释这些现象,并且与动脉的功能特性相符。 MLCK在调节VSM中Ca2 +进入的途径中可能参与了本综述。

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