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JCI table of contents: April 22, 2008
Date:4/22/2008

Diego, San Diego, California, USA.
Phone: (619) 543-6163; E-mail: ddkain@ucsd.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=32691

ACCOMPANYING COMMENTARY
TITLE: Linking adiponectin to proteinuria

AUTHOR CONTACT:
Rexford S. Ahima
University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.
Phone: (215) 573-1872; Fax: (215) 573-5809; E-mail: ahima@mail.med.upenn.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=35655


HEMATOLOGY: A novel role for the protein CD36 in disease-causing blood clot formation

A key step in the formation of a blood clot is the activation and aggregation of cells known as platelets. If a blood clot forms in an intact blood vessel it is known as a thrombus and it can have serious consequences (such as heart disease and stroke) as it restricts, and sometimes even completely blocks, the flow of blood through the vessel. New data, generated by Roy Silverstein and colleagues, at the Cleveland Clinic, has revealed a role for the protein CD36 on platelets in thrombus formation in mice, leading to the suggestion that it might provide a useful new target for the development of anti-thrombotic drugs.

Microparticles are small particles released from cells when they become activated or undergo a form of death known as apoptosis. Physiologically, this means that they are released into the circulation when a blood vessel is injured. In the study, CD36 was shown to mediate binding of human platelets to microparticles derived in vitro from the cells that would be damaged by blood vessel injury and to microparticles isolated from healthy people. Further analysis indicated that CD36
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Contact: Karen Honey
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Journal of Clinical Investigation
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