Prostaglandin E receptors as inflammatory therapeutic targets for atherosclerosis

Abstract Prostaglandin E receptors (EPs) are the G-protein-coupled receptors (GPCRs) that respond to type E 2 prostaglandin (PGE 2 ). Data has shown that PGE 2 may function as an endogenous anti-inflammatory mediator by suppressing the production of cytokines. However, other studies have demonstrated that PGE 2 , a pro-inflammatory mediator produced by various cell types within the wounded vascular wall, plays a crucial role in early atherosclerotic development. These contradictory results may be due to the versatility of EPs. Experimental data suggest an individual role for each PGE 2 receptor, such as EP 1 , EP 2 , EP 3 and EP 4 , in atherosclerosis. In this review, the roles of EPs in atherosclerosis are summarized, and the value of EPs as new therapeutic targets for atherosclerosis is explored.