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Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:388-396
Published online before print January 30, 2003, doi: 10.1161/01.ATV.0000058401.34021.D4
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:388.)
© 2003 American Heart Association, Inc.

ATVB In Focus

Platelet Activation and the Formation of the Platelet Plug

Deficiency of ADAMTS13 Causes Thrombotic Thrombocytopenic Purpura

Han-Mou Tsai

From the Division of Hematology, Montefiore Medical Center and Albert Einstein College of Medicine, Bronx, NY.

Correspondence to Han-Mou Tsai, MD, Montefiore Medical Center, Division of Hematology, 111 E 210th St, Bronx, NY. E-mail htsai{at}montefiore.org

Abstract

In the circulation, a plasma metalloprotease, ADAMTS13, cleaves von Willebrand factor (vWF) in a shear-dependent manner. This article reviews the role of this cleavage in regulating vWF-platelet interaction and proposes a scheme for understanding how a deficiency of ADAMTS13 results in the development of microthrombi in patients with thrombotic thrombocytopenic purpura.


Key Words: von Willebrand factor • thrombotic thrombocytopenic purpura • ADAMTS13 • shear stress • von Willebrand factor cleaving protease




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