Overview of pathophysiology mechanisms in thrombotic APS. ApoER2, apolipoprotein E receptor 2; EMPs, endothelial microparticles; eNOS, endothelial nitric oxide synthase; GPIIb/IIIa, glycoprotein IIb/IIIa; mTOR, mammalian target of rapamycin; NETs, neutrophil extracellular traps; PAR, protease-activated receptor; PF4, platelet factor 4; PI3K, phosphatidylinositol 3-kinase; PSGL-1, P-selectin glycoprotein ligand 1; Ras-ERK, Ras-extracellular signal-related kinase; TF, tissue factor; TLR, toll-like receptor; TXB2, thromboxane B2; VCAM-1, vascular cell adhesion molecule 1; VEGF, vascular endothelial growth factor.