Current topics in the regulatory mechanism underlying the Ca2+ sensitization of the contractile apparatus in vascular smooth muscle
Current topics in the regulatory mechanism underlying the Ca2+ sensitization of the contractile apparatus in vascular smooth muscle
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DOI：
10.1254/jphs.cp0070027
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发表时间：
2007-06-01
影响因子：
3.5
通讯作者：
Hirano, Katsuya
中科院分区：
文献类型：
--
作者：
Hirano, Katsuya
Ca 2+信号是血管平滑肌收缩的主要决定因素。然而，收缩器的Ca 2+敏感性的改变也起着至关重要的作用。肌球蛋白轻链磷酸酶（MLCP）活性的调节被认为是调节Ca 2+敏感性的最重要机制。过去15年的研究已经鉴定出许多参与MLCP活性调节的蛋白质。最近，Ca 2+信号也被证明与调节Ca 2+敏感性的机制相互作用。因此，Rho激酶、蛋白激酶C、CPI-17和MYPT 1都被认为在MLCP活性的调节中发挥生理学上重要的作用。我们现在接近阐明调节MLCP活性和血管收缩过程中Ca 2+敏感性的主要规则。本文将概述目前对MLCP活性调节的生化基础的理解，同时从生理学的角度讨论它们的功能作用。我希望本文将有助于开发新的药理学策略来预防和治疗血管疾病中常见的病理性血管收缩。
The Ca2+ signal is the primary determinant of the contraction of the vascular smooth muscle. However, the alteration of the Ca2+ sensitivity of the contractile apparatus also plays an essential role. The regulation of the myosin light chain phosphatase (MLCP) activity is considered to be the most important mechanism underlying the regulation of Ca2+ sensitivity. The investigations during the last 15 years have identified many proteins that participate in the regulation of the MLCP activity. Recently, the Ca2+ signal has also been shown to cross-talk with the mechanisms regulating the Ca2+ sensitivity. Consequently, Rho kinase, protein kinase C, CPI-17, and MYPT1 have all been suggested to play a physiologically important role in the regulation of the MLCP activity. We are now close to elucidating the major rules regulating the MLCP activity and the Ca2+ sensitivity during vascular contractions. This article will give an overview of the current understanding of the biochemical basis for the regulation of the MLCP activity, while also discussing their functional roles from a physiological point of view. I hope this article will help to develop new pharmacological strategies for the prevention and treatment of the pathological vasoconstriction often seen in vascular diseases.