Key result
EP4 receptor targeting shows preclinical rationale for modulating platelet aggregation without clinical outcome data.
Why the study?
The role of the prostaglandin E2 receptor EP4 in modulating platelet aggregation and its signalling mechanisms is largely unknown despite its potential relevance in cardiovascular thrombosis.
Answers are grounded in this paper and cite their sources.
EP4 platelet modulation lacks clinical evidence; leaves open its viability as antithrombotic target.
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.
No takes yet. Share an insight, caveat, or question.
Philipose et al. (2010) studied Acute myocardial infarction. Prostaglandin E2 receptor EP4 was evaluated on Platelet aggregation. The abstract outlines the rationale for investigating the prostaglandin E2 receptor EP4 as a modulator of platelet aggregation, but reports no clinical results.
Synapse has enriched 10 related papers. Consider them for comparative context: