Acute liver injury (ALI), that is, the development of reduced liver function in patients without preexisting liver disease, can result from a wide range of causes, such as viral or bacterial infection, autoimmune disease, or adverse reaction to prescription and over-the-counter medications. ALI patients present with a complex coagulopathy, characterized by both hypercoagulable and hypocoagulable features. Similarly, ALI patients display a profound dysregulation of the fibrinolytic system with the vast majority of patients presenting with a hypofibrinolytic phenotype. Decades of research in experimental acute liver injury in mice suggest that fibrinolytic proteins, including plasmin(ogen), plasminogen activators, fibrinolysis inhibitors, and fibrin(ogen), can contribute to initial hepatotoxicity and/or stimulate liver repair. This review summarizes major experimental findings regarding the role of fibrinolytic factors in ALI from the last approximately 30 years and identifies unanswered questions, as well as highlighting areas for future research.

急性肝损伤（ALI），即未患有肝病的患者出现肝功能下降，可能由多种原因引起，例如病毒或细菌感染、自身免疫性疾病、处方不良反应和过度服用药物。非处方药。ALI 患者患有复杂的凝血病，其特征是高凝和低凝特征。同样，ALI 患者表现出严重的纤溶系统失调，绝大多数患者呈现纤溶低下表型。数十年对小鼠实验性急性肝损伤的研究表明，纤溶蛋白，包括纤溶酶（原）、纤溶酶原激活剂、纤溶抑制剂和纤维蛋白（原），可导致初始肝毒性和/或刺激肝脏修复。这篇综述总结了过去大约 30 年有关纤溶因子在 ALI 中的作用的主要实验结果，并确定了尚未解答的问题，并强调了未来研究的领域。