Coagulation is controlled by a delicate balance of prothrombotic and antithrombotic mechanisms, to prevent both excessive blood loss from injured vessels and pathologic thrombosis. The liver plays a pivotal role in hemostasis through the synthesis of plasma coagulation factors and their inhibitors that, in addition to thrombosis and hemostasis, orchestrates an array of inflammatory responses. As a result, impaired liver function has been linked with both hypercoagulability and bleeding disorders due to a pathologic balance of pro- and anticoagulant plasma factors. At sites of vascular injury, thrombus propagation that finally may occlude the blood vessel depends on negatively charged biopolymers, such as polyphosphates and extracellular DNA, that provide a physiological surface for contact activation of coagulation factor XII (FXII). FXII initiates the contact system that drives both the intrinsic pathway of coagulation, and formation of the inflammatory mediator bradykinin by the kallikrein–kinin system. Moreover, FXII facilitates receptor-mediated signalling, thereby promoting mitogenic activities, angiogenesis, and neutrophil stimulation with implications for liver diseases. Here, we summarize current knowledge on the FXII-driven contact system in liver diseases and review therapeutic approaches to target its activities during impaired liver function.

凝血受促血栓形成和抗血栓形成机制的微妙平衡控制，以防止受伤血管过度失血和病理性血栓形成。肝脏通过合成血浆凝血因子及其抑制剂在止血中发挥着关键作用，除了血栓形成和止血之外，它们还协调一系列炎症反应。因此，由于促凝和抗凝血浆因子的病理平衡，肝功能受损与高凝状态和出血性疾病有关。在血管损伤部位，最终可能阻塞血管的血栓传播取决于带负电荷的生物聚合物，例如多磷酸盐和细胞外 DNA，它们为凝血因子 XII (FXII) 的接触激活提供生理表面。FXII 启动接触系统，驱动凝血的内在途径和激肽释放酶-激肽系统形成炎症介质缓激肽。此外，FXII 促进受体介导的信号传导，从而促进有丝分裂活性、血管生成和中性粒细胞刺激，从而对肝脏疾病产生影响。在这里，我们总结了目前关于肝病中 FXII 驱动的接触系统的知识，并回顾了在肝功能受损期间针对其活动的治疗方法。和中性粒细胞刺激对肝脏疾病有影响。在这里，我们总结了目前关于肝病中 FXII 驱动的接触系统的知识，并回顾了在肝功能受损期间针对其活动的治疗方法。和中性粒细胞刺激对肝脏疾病有影响。在这里，我们总结了目前关于肝病中 FXII 驱动的接触系统的知识，并回顾了在肝功能受损期间针对其活动的治疗方法。