title: P2Y12 receptor inhibition and LPS-induced coagulation.
abstract: Platelets play a major role in the complex interactions involved in blood coagulation via multiple mechanisms. As reported in this issue, Schoergenhofer et al. tested the hypothesis that platelet inhibition by prasugrel, a potent platelet P2Y12 ADP receptor antagonist, attenuates the effect of lipopolysaccharide (LPS) on the blood coagulation system in healthy human subjects. LPS, a bacterial product with potent pro-inflammatory and pro-thrombotic effects, plays a central role in sepsis. It activates monocytes and endothelial cells via Toll-like receptor (TLR) 4 and other TLRs to stimulate production of TF and other pro-coagulant molecules, chemokines and cytokines. Treatment with prasugrel did not decrease biomarkers of coagulaion. A better understanding of the relative roles of platelet and coagulation mechanisms in triggering the pro-thrombotic state may lead to more effective antithrombotic strategies.
authors: Sol Sherry Thrombosis Research Center and the Division of Hematology, Department of Medicine, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A. david.essex@temple.edu.
authors: David W
authors: DW
authors: Essex
authors: Sol Sherry Thrombosis Research Center and the Division of Hematology, Department of Medicine, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
authors: A Koneti
authors: AK
authors: Rao
mesh_terms: D001777:Blood Coagulation / Q000187:drug effects*; D006801:Humans; D008297:Male; D015539:Platelet Activation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D000068799:Prasugrel Hydrochloride / Q000494:pharmacology*; D058921:Purinergic P2Y Receptor Antagonists / Q000494:pharmacology*
chemical_list: D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D000068799:Prasugrel Hydrochloride
keywords: TLR4; platelets; prasugrel; tissue factor