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.
Commentary| February 04 2016
P2Y12 receptor inhibition and LPS-induced coagulation
David W. Essex;
*Sol Sherry Thrombosis Research Center and the Division of Hematology, Department of Medicine, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
Correspondence: Professor David Essex (email email@example.com).
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David W. Essex, A. Koneti Rao; P2Y12 receptor inhibition and LPS-induced coagulation. Clin Sci (Lond) 1 March 2016; 130 (6): 441–442. doi: https://doi.org/10.1042/CS20150886
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