Applying the brakes to platelet activation

Abstract

In this issue of Blood, Gegenbauer and colleagues provide a new insight into the regulatory mechanisms that allow platelets to produce an optimal response to vascular injury.1 "Optimal responsiveness" in the context of hemostasis means preventing circulating platelets from activating needlessly, allowing them to respond quickly when necessary and limiting platelet activation to avoid excessive platelet accumulation. How all of this is achieved is still not fully understood, but the new study nicely pulls together older work on the classic restrainers of platelet activation (endothelium-derived PGI2 and NO) with emerging ideas about the role of RGS proteins (regulators of G protein signaling). © 2011 by The American Society of Hematology.