Aspirin-triggered 15-epi-lipoxin A4 signals through FPR2/ALX in vascular smooth muscle cells and protects against intimal hyperplasia after carotid ligation

The benefit of aspirin is well established in cardiovascular prevention, and involves the irreversible inhibition of platelet cyclooxygenase (COX)-1 and, as a consequence, decreased thromboxane levels [1]. In addition to inhibition of platelet aggregation, aspirin may also have anti-inflammatory properties, with potential additional benefit in atherosclerosis prevention. Acetylation of the COX-2 enzyme by aspirin directs the metabolism of polyunsaturated fatty acids (PUFAs) towards a biosynthetic pathway, which in addition involves lipoxygenase enzymes and leads to the formation of specific mediators, such as 15-epi-lipoxin A4, also referred to as aspirin-triggered lipoxin (ATL) [2].