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(Circulation Research. 2006;99:1293.)
© 2006 American Heart Association, Inc.

Reviews

Activation of Platelet Function Through G Protein–Coupled Receptors

Stefan Offermanns

From the Institute of Pharmacology, University of Heidelberg, Germany.

Correspondence to Stefan Offermanns, Institute of Pharmacology, University of Heidelberg, Im Neuenheimer Feld 366, 69120 Heidelberg, Germany. E-mail stefan.offermanns{at}pharma.uni-heidelberg.de

This Review is part of a thematic series on Mechanisms, Models, and In Vivo Imaging of Thrombus Formation, which includes the following articles:

Activation of Platelet Function Through G Protein–Coupled Receptors

Platelets As Immune Cells: Bridging Inflammation and Cardiovascular Disease

In Vivo Thrombus Formation

Platelet Adhesion

Platelet Inhibitors and Thrombus Formation
Bernhard Nieswandt and Ulrich Walter Guest Editors

Because of their ability to become rapidly activated at places of vascular injury, platelets are important players in primary hemostasis as well as in arterial thrombosis. In addition, they are also involved in chronic pathological processes including the atherosclerotic remodeling of the vascular system. Although primary adhesion of platelets to the vessel wall is largely independent of G protein–mediated signaling, the subsequent recruitment of additional platelets into a growing platelet thrombus requires mediators such as ADP, thromboxane A₂, or thrombin, which act through G protein–coupled receptors. Platelet activation via G protein–coupled receptors involves 3 major G protein–mediated signaling pathways that are initiated by the activation of the G proteins G_q, G₁₃, and G_i. This review summarizes recent progress in understanding the mechanisms underlying platelet activation and thrombus extension via G protein–mediated signaling pathways.

Key Words: platelet activation • heterotrimeric G proteins • GPCRs • thrombosis

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