Figure 2.

Mechanism of PS⁺ MPs promoting thrombosis after endothelial cells injury. (A) When endothelial cells are damaged, the two ATP-dependent enzymes are unable to function due to energy depletion. However, as intracellular Ca²⁺ concentration, the activated scramblase flips PS to the outer membrane where it initiates coagulation PS provides a scaffold for the activity of factors VIII and V, which binding membranes through their C2 domains, and factors II, VII, IX, and X, which bind using their Gla domains. These factors combine to form the intrinsic (FXIa-FVIIIa-Ca²⁺-PL) factor X enzyme complex and the prothrombin complex (FXa-FVa-Ca²⁺-PL) Damaged endothelial cells can also upregulate the expression of tissue factor, which is activated in the presence of membrane PS and then forms the TF-VIIa complex that participates in exogenous coagulation. (B) SARS-CoV-2 causes endothelial dysfunction and thrombosis. After endothelial cell injury, stimulated platelets were transformed from the resting state to the activated state, and PS⁺ microparticles were released from the surface of endothelial cells to form a particle storm. Platelet adhesion, coupled with PS exposure, stimulates the activation of the clotting cascade, which ultimately leads to thrombosis (The involvement of neutrophils and Nets in endothelial cell injury and thrombosis is also shown in B).