连接蛋白43磷酸化及其信号通路在脓毒症发生机制中的作用研究进展

Research progress on the role of connexin 43 phosphorylation and its signal pathway in the pathogenesis of sepsis

重症监护病房(ICU)患者死亡的主要原因是脓毒症,脓毒症及脓毒性休克严重影响患者的预后,增加了患者的病死率和再次发病率,早期、及时的干预可以降低脓毒症患者的病死率及复发率。脓毒症的发生可能与连接蛋白43(Cx43)的磷酸化有关,而Cx43的磷酸化需要通过各种信号通路实现。Cx43的相关位点通过不同信号通路发生磷酸化,实现了对脓毒症的精准调节,这些位点可能成为治疗脓毒症的相关靶点,为精准化治疗脓毒症提供方向。本文主要分析蛋白激酶A(PKA)、蛋白激酶C(PKC)、丝裂素活化蛋白激酶(MAPK)及磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/Akt)等与Cx43相关的信号通路在脓毒症发生机制中的作用。

Sepsis is the main cause of death in intensive care unit(ICU).Sepsis and septic shock seriously affect the prognosis of patients and increase the mortality and re-morbidity of patients.Early and timely intervention can reduce the mortality and recurrence rate of patients with sepsis.The occurrence of sepsis may be related to the phosphorylation of connexin 43(Cx43),which needs to be realized through various signal pathways.The related sites of connexin 43 are phosphorylated through different signal pathways to achieve the precise regulation of sepsis,these sites may be related targets for the treatment of sepsis and provide a direction for accurate treatment of sepsis.This paper mainly analyzes the role of Cx43-related signal pathways such as protein kinase A(PKA),protein kinase C(PKC),mitogen-activated protein kinase(MAPK)and phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)in the pathogenesis of sepsis.