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Arteriosclerosis, Thrombosis, and Vascular Biology
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Published Online
on January 3, 2008

Arteriosclerosis, Thrombosis, and Vascular Biology. 2008
Published online before print January 3, 2008, doi: 10.1161/ATVBAHA.107.161026
A more recent version of this article appeared on March 1, 2008
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*Blood Thinners

Submitted on December 13, 2007
Accepted on December 19, 2007

Novel Therapeutic Targets at the Platelet-Vascular Interface for Arteriosclerosis, Thrombosis, and Vascular Biology

Lawrence F. Brass *; Li Zhu ; and Tim Stalker

From the University of Pennsylvania, Department of Medicine, Division of Hematology-Oncology, Philadelphia.

* To whom correspondence should be addressed. E-mail: Brass{at}mail.med.upenn.edu.

Abstract—Platelet activation in vivo can be part of the hemostatic response to injury or a pathological response to disease. In either setting, platelets adhere to the vessel wall and to each other, forming a closely packed mass interspersed with fibrin. Recent studies have identified new molecules on the platelet surface and within platelets that support and regulate thrombus growth and stability, ensuring that platelet accumulation after injury is sufficient to stop bleeding, but not so exuberant that vascular occlusion occurs. An understanding of how this balance is achieved helps to illuminate the events of platelet activation and, at the same time, provides potential targets for new classes of antiplatelet agents.


Key words: platelets • cell adhesion molecules • integrins • semaphorins • ephrins • Eph kinases • vascular biology




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