| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3029372 | Thrombosis Research | 2010 | 7 Pages |
Abstract
There is significant interindividual variation of platelet response to PGE2 in humans. The balance between EP2, EP3, and EP4 activation determines its net effect. PGE2 can prevent thromboxane-induced platelet aggregation in an EP4-dependent manner. EP3 antagonism converts platelets of nonresponders to a PGE2-responsive phenotype. These data suggest that therapeutic targeting of EP pathways may have cardiovascular benefit by decreasing platelet reactivity.
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Authors
James P. Smith, Elias V. Haddad, Jason D. Downey, Richard M. Breyer, Olivier Boutaud,