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This editorial refers to ‘Vessel wall, not platelet, P2Y12 potentiates early atherogenesis’ by L.E. West et al. , doi:10.1093/cvr/cvu028. Platelets play a key role in primary haemostasis and also represent an important interface between thrombosis, immunity, and atherogenesis.1 Platelet-triggered inflammatory pathways contribute to the formation of atherosclerotic lesions and atherothrombosis. Platelets express receptors for a variety of agonists that initiate platelet activation, which is then amplified and sustained by activation of the G-protein-coupled purinergic receptor P2Y12. P2Y12 mediates platelet aggregation and secretion of platelet granule contents in response to ADP.2 P2Y12 is also a well-established target for anti-thrombotic drugs, such as the thienopyridine compounds ticlopidine, clopidogrel, and prasugrel or the direct, reversible antagonists ticagrelor, cangrelor, and elinogrel.2 Clinical studies have shown that in addition to preventing arterial thrombus formation in patients with coronary artery syndromes or after stent implantation, anti-thrombotic/anti-platelet therapy is also associated with systemic anti-inflammatory effects.3 While these findings imply an important role for P2Y12 in the regulation of platelet functions, P2Y12 expression is not restricted to platelets. Indeed, accumulating data indicate that P2Y12 may directly mediate pro-inflammatory and atherogenic actions in the vessel wall apparently independently of platelet activation. West et al. 4 provide evidence supporting this notion by describing a role for vessel wall, but not platelet, P2Y12 in the development of early atherosclerotic lesions.West et al. utilized the well-established ApoE-deficient mice model of atherosclerosis and generated ApoE−/−P2Y12−/− (DK) mice by back-crossing P2Y12-deficient mice into ApoE−/− mice. Using homologous and …

Purinergic receptors and atherosclerosis: emerging role for vessel wall P2Y12