摘要
凝血功能障碍是脓毒症患者常见的并发症，导致病死率显著增加。高迁移率族蛋白B1（HMGB1）作为一种“晚期”炎症因子，介导了脓毒症相关凝血功能障碍（SIC）的发生发展。释放进入血液的HMGB1可导致机体出现高凝状态，诱发弥散性血管内凝血（DIC）形成，并导致多器官衰竭。因此，干预HMGB1可能作为SIC的潜在治疗靶点。本文对HMGB1介导SIC的作用机制及各种潜在的治疗进行综述，为进一步防治SIC提供方向。
Abstract
Coagulation dysfunction is a common complication in septic patients, leading to a significant increase in mortality. High mobility group box protein 1 (HMGB1), as a late inflammatory cytokine, mediates the occurrence and development of sepsis-induced coagulopathy. HMGB1 released into blood can cause hypercoagulability, inducing formation of disseminated intravascular coagulation, and leading to multiple organ failure. Therefore, intervention of HMGB1 may serve as a potential therapeutic target for sepsis-induced coagulopathy. This paper reviews the mechanism by which HMGB1 mediated sepsis-induced coagulopathy, as well as current approaches and clinical potential of HMGB1-targeting strategies, with the goal of providing the directions for the treatment of sepsis-induced coagulopathy.
基金项目
国家自然科学基金面上项目(81870066)
江苏省科技厅重点研发(社发)项目(BE2020786)
江苏省第六期“333高层次人才培养工程”第二层次人才项目()
万方数据