Signal transduction and regulation in smooth muscle
Signal transduction and regulation in smooth muscle
复制标题
DOI：
10.1038/372812a0
复制
发表时间：
1994-12
期刊：
影响因子：
64.8
通讯作者：
A. Somlyo;A. Somlyo
中科院分区：
文献类型：
--
作者：
A. Somlyo;A. Somlyo
许多器官壁上的平滑肌细胞对大多数身体功能至关重要，它们的异常会导致一系列疾病。尽管平滑肌的收缩机制与横纹肌类似，但平滑肌的收缩是由药物力学和机电耦合机制调节的。最近的研究揭示了以前未被认识到的收缩调节过程，如g蛋白偶联抑制肌球蛋白轻链磷酸酶，其他激酶对肌球蛋白轻链激酶的调节，以及平滑肌肌球蛋白亚型的功能作用。这些调节机制的异常和异构体变异可能导致平滑肌疾病，g蛋白偶联抑制蛋白磷酸酶也可能在调节细胞质肌球蛋白II介导的非肌肉细胞功能中起重要作用。
Smooth muscle cells in the walls of many organs are vital for most bodily functions, and their abnormalities contribute to a range of diseases. Although based on a sliding-filament mechanism similar to that of striated muscles, contraction of smooth muscle is regulated by pharmacomechanical as well as by electromechanical coupling mechanisms. Recent studies have revealed previously unrecognized contractile regulatory processes, such as G-protein-coupled inhibition of myosin light-chain phosphatase, regulation of myosin light-chain kinase by other kinases, and the functional effects of smooth muscle myosin isoforms. Abnormalities of these regulatory mechanisms and isoform variations may contribute to diseases of smooth muscle, and the G-protein-coupled inhibition of protein phosphatase is also likely to be impor-tant in regulating non-muscle cell functions mediated by cytoplasmic myosin II.