{"title":"[Research progress of neutrophil extracellular traps in septic coagulopathy].","authors":"Zhuowen Dai, Qiong Wang","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Sepsis-induced coagulopathy (SIC) ranks among the most dangerous coagulation disorders in intensive care units, with an incidence rate of up to 67.9% in China. This high mortality is mainly attributed to vascular endothelial cell injury and coagulation dysfunction caused by sepsis. Neutrophil extracellular traps (NETs) are reticular complexes formed by activated neutrophils in infected organisms through the release of DNA, proteases, cytokines, and other components. Recent studies have demonstrated that NETs can trigger systemic hemostatic imbalance in sepsis patients by mediating vascular endothelial damage, promoting immunothrombosis, and disrupting the coagulation-fibrinolysis balance, ultimately leading to the development of SIC. Therefore, this article reviews the mechanistic role of NETs in SIC and discusses recent advances in their potential as diagnostic biomarkers and therapeutic targets.</p>","PeriodicalId":61378,"journal":{"name":"细胞与分子免疫学杂志","volume":"42 8","pages":"749-754"},"PeriodicalIF":0.0000,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"细胞与分子免疫学杂志","FirstCategoryId":"3","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Sepsis-induced coagulopathy (SIC) ranks among the most dangerous coagulation disorders in intensive care units, with an incidence rate of up to 67.9% in China. This high mortality is mainly attributed to vascular endothelial cell injury and coagulation dysfunction caused by sepsis. Neutrophil extracellular traps (NETs) are reticular complexes formed by activated neutrophils in infected organisms through the release of DNA, proteases, cytokines, and other components. Recent studies have demonstrated that NETs can trigger systemic hemostatic imbalance in sepsis patients by mediating vascular endothelial damage, promoting immunothrombosis, and disrupting the coagulation-fibrinolysis balance, ultimately leading to the development of SIC. Therefore, this article reviews the mechanistic role of NETs in SIC and discusses recent advances in their potential as diagnostic biomarkers and therapeutic targets.