Figure 2.

Schematic overview of potential therapeutic targets to prevent monocyte-platelet interactions. Depicted are G protein-coupled receptors (GPCR) associated with platelet receptors P2Y₁₂ and PAR1 as well as GPIIb/IIIa receptors on the platelet surface, and cyclooxygenase-1 (COX-1)-mediated production of platelet-activating thromboxane A2. Following platelet activation, many interconnected pathways result in intracellular calcium increase, activation of GPIIb/IIIa, and release of alpha and dense granule contents. P-selectin (released from alpha granules) translocates to the platelet surface and binds to P-selectin glycoprotein ligand-1 (PSGL1) on the monocyte surface, resulting in monocyte-platelet aggregates (MPA). In turn, monocytes become proinflammatory and procoagulant. *has received a conditional marketing authorization by the European Medicines Agency in 2020. Figure created with BioRender.com