1,4,5-三磷酸肌醇受体及其在休克中的作用  

Inositol 1,4,5-trisphosphate receptor and its role during shock

作　　者：张立霞 牛春雨[1] 赵自刚[1] Zhang Lixia;Niu Chunyu;Zhao Zigang(Institute of Microcirculation,Hebei North University,Zhangjiakou 075000,China)

机构地区：[1]河北北方学院微循环研究所,河北张家口075000

出　　处：《中国急救医学》2024年第7期639-644,共6页Chinese Journal of Critical Care Medicine

基　　金：国家自然科学基金(81670446)。

摘　　要：1,4,5-三磷酸肌醇(IP3)受体(IP3R)是内质网释放钙离子(Ca2+)的主要通道之一,在维持细胞内钙稳态方面发挥着重要作用。休克作为一种严重的、发生器官功能障碍与结构损伤的病理过程,钙稳态失调是其重要的中间环节。鉴于IP3R功能或表达异常引起钙稳态失调参与了多种病理过程的发生、进展,本文对IP3R结构与调节的研究进展进行综述,总结IP3R在失血性休克、感染性休克中的作用,期望以IP3R为切入点,为防治重症休克提供理论基础,并探索靶向IP3R防治休克的新策略。The inositol 1,4,5-trisphosphate receptor(IP3R)is the one of primary channels responsible for the release of calcium ions(Ca 2+)from the endoplasmic reticulum,playing a vital role in maintaining intracellular calcium homeostasis.The imbalance of calcium homeostasis is an important intermediate link of shock-induced organ dysfunction and structural damage,which is a severe pathological process.The imbalance of calcium homeostasis induced by the dysfunction and abnormal expression of IP3R which participates in the occurrence and progress of various pathological process,this article reviews the advancements of IP3R construction and regulation,summarizes the role of IP3R during hemorrhagic shock and septic shock.Basing on this,we hope to provide a theoretical basis for the prevention and treatment of severe shock,and explore new strategies targeting IP3R.

关 键 词：1 4 5-三磷酸肌醇受体 钙稳态 内质网应激 失血性休克 感染性休克 

分 类 号：R459.7[医药卫生—急诊医学]