Fig. 3

The property of endothelial cells after glycocalyx denudation in sepsis. Intact vascular endothelial cells maintain their antithrombogenicity through various mechanisms, including the production of nitric oxide (NO), prostacyclin (prostaglandin I₂, PG I₂), secretion of angiopoietin-1 (Ang1), and expression of thrombomodulin (TM), which facilitates the conversion of protein C (PC) to its active form, activated protein C (APC), in the presence of thrombin. However, in sepsis, the endothelium's antithrombotic properties are compromised. This shift occurs due to the expression of tissue factor (TF), the release of angiopoietin-2 (Ang2), and disruption of the glycocalyx. Thromboinflammation is further exacerbated by the binding of damage-associated molecular patterns (DAMPs) to pattern-recognition receptors (PRRs), thrombin interaction with protease activator receptor 1 (PAR-1), and upregulation of various adhesion molecules. Additionally, the release of von Willebrand factor (vWF) from endothelial cells promotes platelet aggregation. NF-κB: nuclear factor-κB, MVs: microvesicles, ICAM-1: intercellular cell adhesion molecule-1, PSGL-1:P-selectin glycoprotein ligand-1, Macrophage 1 antigen: MAC-1: LFA-1: lymphocyte function-associated antigen-1