血管低反应性是制约创伤休克等临床重症治疗的关键问题，现有研究多关注血管细胞本身及其相关收缩蛋白分子，而细胞器和亚细胞结构功能障碍在其中的作用研究较少。高尔基体应激是近年来发现的一种细胞器自身调节性反应，在疾病过程中发挥重要作用，但它在创伤后心血管功能障碍中的作用尚不清楚。本课题组近期研究发现，高尔基体应激参与了创伤休克后血管低反应性的发生，同时诱导高尔基体应激能降低缝隙连接蛋白Cx43的表达水平。我们推测：高尔基体应激可能通过UBIAD1介导的Ras-MAPK和Rho-ROCK信号通路间交互调节模式调节Cx43来参与创伤休克血管低反应性的调节。据此，本研究拟采用创伤失血休克模型，研究高尔基体应激在休克血管低反应性中的作用，探讨高尔基体应激通过UBIAD1调节Cx43的交互调控机制。希望从一个新的角度解释休克血管低反应性的发生机制，为临床重症的治疗提供新的靶点和防治措施。

Vascular hyporeactivity is crucial for the treatment of critical illness such as severe trauma and shock. The current research focused on the vascular cells themselves and their contractile proteins, but the role of dysfunction of organelle and subcellular structure is less reported. Recent studies showed that Golgi stress is one of the systems of organelle autoregulation and it is linked to many diseases, but the role of Golgi stress in posttraumatic cardiovascular dysfunction after trauma is unclear. Our recently studies found that Golgi stress participated in the incidence of vascular hyporesponsiveness following traumatic shock, and decreased the expression of the gap junction protein Cx43. We hypothesize that Golgi stress may take part in the occurrence of traumatic shock-induced vascular hyporeactivity via UBIAD1-mediated cross-talk between Ras-MAPK and Rho-ROCK pathways. To test this hypothesis, we adopted a model of traumatic hemorrhagic shock, to investigate the role of Golgi stress in traumatic shock-induced vascular hyporeactivity and investigate the mechanism that Golgi stress regulates Cx43 via UBIAD1-mediated cross-talk between Ras and Rho pathways. The main objective tends to explore the new mechanism to explain the occurrence of vascular hyporeactivity, and provide the new therapeutic targets and modulation strategy for clinical critical conditions.