A biological target for antiplatelet therapy: the prostaglandin E2 receptor EP4
نویسندگان
چکیده
Background Acute myocardial infarction is one of the leading causes of death in the world which is caused by coronary artery thrombosis. Platelets play a central role in cardiovascular thrombosis. Platelet aggregation caused due to a ruptured artherosclerotic plaque could eventually lead to vascular occlusion. Another important component of vascular diseases is inflammation. During inflammation, prostaglandins (PG) like PGI2, PGE2 and PGD2 are released which are also involved in thrombosis. Lower concentrations of PGE2 enhance platelet aggregation whereas higher concentrations inhibit aggregation. PGE2 acts via 4 receptors: EP1, EP2, EP3 and EP4 (Gs signalling). The role of the EP3 receptor in enhancing platelet activation and aggregation has been looked at in detail but the role of the EP4 receptor is largely unknown. We were interested in how this receptor modulates platelet aggregation and what are the signalling mechanisms involved in this process.
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عنوان ژورنال:
دوره 10 شماره
صفحات -
تاریخ انتشار 2010