Caldesmon及其磷酸化调节肠道平滑肌收缩舒张功能研究进展

Caldesmon and Its Phosphorylation in Regulating Contraction and Relaxation of Intestinal Smooth Muscle

肠道平滑肌的收缩和舒张与粗细肌丝的调节密切相关。Caldesmon作为一种肌动蛋白结合蛋白,是参与肠道平滑肌粗细肌丝调节的重要收缩蛋白之一,可通过与肌动蛋白、肌球蛋白和原肌球蛋白交联,阻碍肌动蛋白与肌球蛋白的结合,从而抑制肠道平滑肌的收缩。然而,Caldesmon的磷酸化修饰可以逆转这种抑制作用。Caldesmon可以被不同信号通路中的蛋白激酶刺激,引起自身的磷酸化,促进肌动蛋白与肌球蛋白的结合,进一步导致肠道平滑肌的收缩,在肠道动力障碍疾病中起到关键作用。分别以“Caldesmon”、“平滑肌”、“磷酸化”和以“Caldesmon”、“smooth muscle”、“phosphorylation”、“actin”、“myosin”、“contraction and relaxation”为主题词在中国知网(CNKI)、百度学术和PubMed数据库中查找Caldesmon与平滑肌或肠道平滑肌相关文献。该文就Caldesmon及其磷酸化参与调节肠道平滑肌收缩舒张的功能以及介导Caldesmon磷酸化的相关上游信号通路等方面进行综述,旨在为以基于Caldesmon及其磷酸化调节肠道平滑肌收缩舒张为靶点的临床疾病治疗提供理论依据。

The contraction and relaxation of intestinal smooth muscle are closely related to the regulation of thick and thin muscle filaments.As an actin-binding protein,Caldesmon is one of the important contractile proteins involved in the regulation of the thick and thin filaments of intestinal smooth muscle.It can cross-link with actin,myosin and tropomyosin to prevent the binding of actin and myosin,thus inhibiting the contraction of the intestinal smooth muscle.However,phosphorylation modifications of Caldesmon can reverse this inhibition.Caldesmon plays a key role in intestinal motility disorders,and can be stimulated by protein kinase activated through different signaling pathways to cause its own phosphorylation,thereby enhancing the binding of actin and myosin,and further causing the contraction of intestinal smooth muscle.In CKNI,Baidu Academic and PubMed databases,