RhoA/ROCK信号通路对血管平滑肌收缩的调节作用及研究进展

Regulation of RhoA/ROCK pathway on vascular smooth muscle contraction and its recent research

血管平滑肌的异常收缩是引起许多疾病的重要因素,如高血压,脑血管痉挛等,对于平滑肌收缩调节机制的研究为治疗这些疾病带来新的思路和方向。研究表明小GTP结合蛋白RhoA及其下游信号分子ROCK在平滑肌收缩调节,尤其是钙敏化调节机制中起到关键作用。RhoA/ROCK通路通过抑制MLCP活性而增强MLC的磷酸化水平,从而调节平滑肌收缩,此外,它还参与调节其它细胞的多种细胞功能,如应力纤维的生成,细胞分裂及迁移等。本综述主要介绍RhoA/ROCK通路在血管平滑肌收缩功能的调节机制及研究进展。

The abnormal contraction of vascular smooth muscle is a key cause of many disases such as hypertension and vasospasm of the cerebral arteries.The research of the mechanism of regulation of smooth muscle contraction shoule lead to new mind for such diseases.Recent research reveal the major function of the small GTP-binding protein RhoA and its downstream effector,ROCK in the regulation of smooth muscle contraction,especially in Ca2＋ sensitization mechanism.The RhoA/ROCK pathway could increase MLC phosphorylation by inhibiting the activity of MLCP,and then lead to smooth muscle contraction.In addition,it also participate in a variety of the cellular functions of other cells,such as stress-fibre formation,cytokinesis and cell migration.We review the modulatory role of RhoA/ROCK pathway in vascular smooth muscle contraction and its recent perspecitive.