The critical role of G protein–coupled receptor kinase 2 (GRK2) in regulating cardiac
function has been well documented for> 3 decades. Targeting GRK2 has therefore been
extensively studied as a novel approach to treating cardiovascular disease. However, little is
known about its role in hemostasis and thrombosis. We provide here the first evidence that
GRK2 limits platelet activation and regulates the hemostatic response to injury. Deletion of
GRK2 in mouse platelets causes increased platelet accumulation after laser-induced injury …

Abstract Venous thromboembolism (VTE), heart attack, and stroke are all diseases in which
platelets play a role, through inappropriate platelet activation and subsequent thrombus
formation. Most platelet agonists activate platelets via G protein-coupled receptors (GPCRs),
which are targeted by many antiplatelet drugs. Along with thrombin and TxA 2, ADP has long
been recognized for its important role in hemostasis and thrombosis. It activates platelets via
GPCRs, P2Y 1 and P2Y 12. However, little is known about the negative feedback …