Figure 2.
Mechanisms of aPL-mediated thrombosis and inhibition by warfarin or DOAC. This figure depicts multiple potential mechanisms underlying APS and the cell types that are affected by aPL. Cellular activation results in cell-specific responses that include releases of neutrophils extracellular traps (NETs), expression of cellular procoagulant activity, and extracellular vesicle release, among others. Warfarin inhibits γ-carboxylation of vitamin K–dependent coagulation factors, thus reducing the catalytic efficiency of coagulation complexes such as the phospholipid-dependent tenase and prothrombinase reactions.