Fig. 2

The degradation of endothelial glycocalyx in sepsis. Activated monocytes initiate both extrinsic and intrinsic coagulation pathways by expressing tissue factor (TF) and phosphatidylserine (PS). Simultaneously, neutrophils are activated by proinflammatory cytokines and ultimately undergo cell death, leading to extracellular trap formation. Intravascular thromboinflammation results in endothelial activation, leading to hypofibrinolysis due to increased production of plasminogen activator inhibitor 1 (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI). Thromboinflammation, increased shedders, and hyperglycemia in sepsis also damage the glycocalyx. Moreover, treatments for sepsis and septic shock, such as volume overload and excessive catecholamine administration, further exacerbate glycocalyx damage