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Fig. 3 | Journal of Inflammation

Fig. 3

From: Neutrophil extracellular traps in acute coronary syndrome

Fig. 3

Schematic illustration of molecular mechanisms of neutrophil extracellular traps (NETs) in atherosclerosis. When the inducer stimulates neutrophils, they are activated to produce NETs, which participate in the formation of atherosclerosis through the expression of related molecules. Additionally, NETs promote the adhesion and aggregation of platelets and the binding of red blood cells through two coagulation pathways, providing a physical scaffold for thrombus growth. Furthermore, NETs also damage the endothelium through the joint action of IL-1 and cathepsin G, thereby promoting the expression of ICAM-1, VCAM-1 and tissue factors, participating in the formation of thrombus and causing the lysis of smooth muscle cells through the exogenous histone H4 and aiding in the easy sloughing of the plaque

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