Fig. 2
From: Oxidative stress in acute pulmonary embolism: emerging roles and therapeutic implications
Partial mechanisms of APE (red font). Under conditions of oxidative stress, endothelial cells become injured, and tissue factors and endothelial microparticles are released to activate leukocytes and platelets. sICAM and E-selectin were abnormally elevated. Meanwhile, leukocytes are overactivated by CINC-1, CINC-2, MCP-1, and MIP-1. Lysophosphatidic acid released by activated platelets stimulates neutrophils to release neutrophil extracellular traps, which promote thrombotic stability. High mobility group box 1 and platelet-derived microparticles also activate neutrophils to trigger venous thrombosis. Besides, the absence of blood flow in shear stress and reperfusion causes damage to endothelial cells via a mechanical signal cascade “sense”. These mechanisms interact to aggravate oxidative stress in APE (APE: acute pulmonary embolism; CINC: cytokine-induced neutrophil chemoattractant; EMP: endothelial microparticle; HMGB: high mobility group box 1; sICAM: soluble intercellular cell adhesion molecule; MCP: monocyte chemotactic protein; MIP: macrophage inflammatory protein; MMP-9: matrix metalloprotein-9; NETs: neutrophil extracellular traps; PDMP: platelet-derived microparticles; TF: tissue factor)