Abstract：
BACKGROUND: Sepsis-associated coagulopathy specifically refers to widespread systemic coagulation activation accompanied by a high risk of hemorrhage and organ damage, which in severe cases manifests as disseminated intravascular coagulation (DIC), or even develops into multiple organ dysfunction syndrome (MODS). The complement system and the coagulation system as the main columns of innate immunity and hemostasis, respectively, undergo substantial activation after sepsis.
CONCLUSIONS: Dysfunction of the complement, coagulation/fibrinolytic cascades caused by sepsis leads to \"thromboinflammation,\" which ultimately amplifies the systemic inflammatory response and accelerates the development of MODS. Recent studies have revealed that massive activation of the complement system exacerbates sepsis-induced coagulation and even results in DIC, which suggests that inhibition of complement activation may have therapeutic potential in the treatment of septic coagulopathy.
CONCLUSIONS: Sepsis-associated thrombosis involves the upregulation or activation of procoagulant factors, down-regulation or inactivation of anticoagulant factors, and impairment of the fibrinolytic mechanism. This review aims to summarize the latest literature and analyze the underlying molecular mechanisms of the activation of the complement system on the abnormal coagulation cascades in sepsis.
CONCLUSIONS: Dysfunction of the complement, coagulation/fibrinolytic cascades caused by sepsis leads to \"thromboinflammation,\" which ultimately amplifies the systemic inflammatory response and accelerates the development of MODS. Recent studies have revealed that massive activation of the complement system exacerbates sepsis-induced coagulation and even results in DIC, which suggests that inhibition of complement activation may have therapeutic potential in the treatment of septic coagulopathy.
CONCLUSIONS: Sepsis-associated thrombosis involves the upregulation or activation of procoagulant factors, down-regulation or inactivation of anticoagulant factors, and impairment of the fibrinolytic mechanism. This review aims to summarize the latest literature and analyze the underlying molecular mechanisms of the activation of the complement system on the abnormal coagulation cascades in sepsis.
摘要：
脓毒症相关性凝血病特别是指广泛的全身凝血激活，伴有出血和器官损伤的高风险，在严重的情况下表现为弥散性血管内凝血（DIC），甚至发展为多器官功能障碍综合征（MODS）。脓毒症后，作为先天免疫和止血主要柱的补体系统和凝血系统分别经历了大量激活。补体功能障碍，脓毒症引起的凝血/纤溶级联反应导致“血栓炎症”，最终放大全身炎症反应并加速MODS的发展。最近的研究表明，补体系统的大量激活会加剧脓毒症诱导的凝血功能，甚至导致DIC，这表明抑制补体激活可能在治疗脓毒性凝血病方面具有治疗潜力。脓毒症相关的血栓形成涉及促凝血因子的上调或激活，抗凝因子下调或失活，和纤溶机制的损害。本综述旨在总结最新文献，分析补体系统激活对脓毒症异常凝血级联反应的潜在分子机制。
