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多种激酶参与钙敏感性调节机制,其中较为重要的有RhoA激酶、酪氨酸激酶和蛋白激酶C。RhoA激酶主要通过抑制肌球蛋白轻链磷酸酶的活性上调肌球蛋白轻链磷酸化水平;酪氨酸激酶可以激活鸟苷酸转换因子,后者促进肌球蛋白轻链19位丝氨酸磷酸化;蛋白激酶C可以促进CPI-17磷酸化,磷酸化的CPI-17可以抑制肌球蛋白磷酸酶。以上情况均可以增加血管平滑肌细胞钙敏感性。在脑血管痉挛的慢性痉挛期,脑血管平滑肌钙敏感性增加与脑血管痉挛的发生发展密切相关。本文对钙敏感性机制和以上三种激酶在脑血管痉挛发病机制中的作用做一综述,以期为防治此类疾病提供新的思路。
A variety of kinases are involved in the mechanism of calcium sensitivity regulation, among which the more important ones are RhoA kinase, tyrosine kinase and protein kinase C. RhoA kinase mainly up-regulates myosin light chain phosphorylation by inhibiting myosin light chain phosphatase activity; tyrosine kinase activates guanylate conversion factor, which promotes serine 19 light chain serine phosphorylation; Protein kinase C can promote CPI-17 phosphorylation, and phosphorylated CPI-17 can inhibit myosin phosphatase. The above conditions can increase the calcium sensitivity of vascular smooth muscle cells. In the chronic spasm of cerebral vasospasm, increased calcium sensitivity of cerebrovascular smooth muscle is closely related to the occurrence and development of cerebral vasospasm. In this paper, the mechanisms of calcium sensitivity and the above three kinases in the pathogenesis of cerebral vasospasm are reviewed in this paper, with a view to providing new ideas for the prevention and treatment of such diseases.