颅脑创伤引起的凝血功能障碍是影响TBI 患者预后的一个重要因素。目前经典的创伤性凝血病发生机制并不能完全解释这一现象。作为启动外源性凝血途径中的核心，血浆中FVIIa水平的高低在很大程度上直接决定了颅脑创伤后机体的凝血状态。在前期研究中，我们发现颅脑创伤后FVIIa活性明显下降。F7基因的多态性和启动子甲基化是否参与颅脑创伤患者凝血功能障碍的发生，目前尚无相关的研究报道。我们将以此为研究重点，全面阐述"F7基因多态性和启动子甲基化决定颅脑创伤后凝血功能状况"的假说，从全新的角度解释TBI 患者凝血功能状态的改变。最后，探讨外源性FVIIa在颅脑创伤后止血的作用机制，着重阐述FVIIa与EPCR结合后激活PAR1介导的细胞信号通路的过程和病理生理意义。从而，为颅脑创伤性凝血功能障碍的早期干预提供理论基础和实践指导。

Coagulopathy caused by traumatic brain injury(TBI) is an important risk affecting the prognosis of TBI patients. The classic traumatic coagulopathy mechanism does not fully explain this phenomenon. As the core of the extrinsic coagulation pathway, plasma FVIIa levels largely determine the coagulation status after TBI. In preliminary study, we found that FVIIa activity of patients was decreased after TBI.It is unknown whether F7 gene polymorphism and promoter methylation are involved in the occurrence of coagulopathy in patients with TBI. We will focus on the regulation mechanism of F7 gene, comprehensively elucidate the hypothesis of "F7 gene polymorphism and promoter methylation determinate the coagulation status of patients after TBI", explain the alteration of coagulation status of patients with TBI from a new perspective. Finally, we will explore the hemostatic mechanism of exogenous FVIIa after TBI, and mainly focus on the PAR1-mediated singal pathway activated by FVIIa combined with EPCR and its pathophysiological significance. Therefore, it will provide a theoretical basis and practical guidance for early intervention for TBI coagulopathy.