Zhu Lei, Dong He, Li Lin, Liu Xiaojie
Department of Anesthesiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, People's Republic of China.
Department of Anesthesiology, Shandong Provincial Key Medical and Heath Laboratory of Anesthesia and Brain Function, Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, People's Republic of China.
J Inflamm Res. 2025 Feb 3;18:1479-1495. doi: 10.2147/JIR.S504184. eCollection 2025.
Sepsis is a critical condition characterized by organ dysfunction due to a dysregulated response to infection that poses significant global health challenges. Coagulation dysfunction is nearly ubiquitous among sepsis patients. Its mechanisms involve platelet activation, coagulation cascade activation, inflammatory reaction imbalances, immune dysregulation, mitochondrial damage, neuroendocrine network disruptions, and endoplasmic reticulum (ER) stress. These factors not only interact but also exacerbate one another, leading to severe organ dysfunction. This review illustrates the mechanisms of sepsis-induced coagulopathy, with a focus on tissue factor activation, endothelial glycocalyx damage, and the release of neutrophil extracellular traps (NETs), all of which are potential targets for therapeutic interventions.
脓毒症是一种危急病症,其特征是由于对感染的反应失调导致器官功能障碍,这对全球健康构成了重大挑战。凝血功能障碍在脓毒症患者中几乎普遍存在。其机制涉及血小板活化、凝血级联反应活化、炎症反应失衡、免疫失调、线粒体损伤、神经内分泌网络破坏以及内质网(ER)应激。这些因素不仅相互作用,还会相互加剧,导致严重的器官功能障碍。本综述阐述了脓毒症诱导的凝血病的机制,重点关注组织因子激活、内皮糖萼损伤和中性粒细胞胞外陷阱(NETs)的释放,所有这些都是治疗干预的潜在靶点。