Fig. 2

Exosomes regulation of sepsis-induced coagulopathy. Exosomes intricately regulate the balance between immune and coagulation responses in the pathophysiology of sepsis-induced coagulopathy. Macrophage-derived exosomes directly exert procoagulant activity, thereby initiating the coagulation cascade. Furthermore, these vesicles significantly influence neutrophil (PMN) recruitment and neutrophil extracellular traps (NETs), effectively linking inflammatory and coagulation pathways. Additionally, platelet-derived exosomes enhance both coagulation and inflammation, which may potentially lead to disseminated intravascular coagulation (DIC) and subsequent organ damage. Endothelial dysfunction can be notably impacted by exosomal signals from various cells, thereby contributing to ongoing inflammation and coagulation. Conversely, exosomes from endothelial progenitor cells (EPCs) play a crucial role in facilitating vascular repair and reducing endothelial permeability, effectively countering the vascular effects of sepsis. This underscores the significant role of exosomes in the development of coagulopathy during sepsis. PS phosphatidylserine, TF tissue factor, HMGB1 high mobility group box 1, ARA arachidonic acid, IL-10 interleukin 10, MMP9 matrix metallopeptidase 9