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Issue 973 coverCELL SIGNALING, TRANSCRIPTION, AND TRANSLATION AS THERAPEUTIC TARGETS Copyright © 2002 by the New York Academy of Sciences
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Articles by NIESSEN, H. W. M.
Articles by HACK, C. E.
Annals of the New York Academy of Sciences 973:573-585 (2002)
© 2002 New York Academy of Sciences

Intercellular Adhesion Molecule-1 in the Heart

HANS W. M. NIESSENa,b, PAUL A. J. KRIJNENa,b, CEES A. VISSERb,c, CHRIS J. L. M. MEIJERa AND C. ERIK HACKb,d,e

aDepartment of Pathology, bICaR-VU, cDepartment of Cardiology, and dDepartment of Clinical Chemistry, VU University Medical Center, Amsterdam, the Netherlands
eDepartment of Immunopathology, Sanquin Research at CLB, Amsterdam, the Netherlands

Address for correspondence: Hans W.M. Niessen, Department of Pathology, VU University Medical Center, Room OE16, De Boelelaan 1117, 1007 MB Amsterdam, the Netherlands. Voice: +31.20.444.4003; fax: +31.20.444.2964.
jwm.niessen{at}vumc.nl
Ann. N.Y. Acad. Sci. 973: 573-585 (2002).

Intercellular adhesion molecule-1 (ICAM-1) belongs to the superfamily of immunoglobulin-like adhesion molecules. Up-regulation of ICAM-1 occurs in many different pathophysiological processes. Also, cardiomyocytes can express ICAM-1—for example, in acute myocardial infarction. Moreover, inhibition of ICAM-1 expression in the heart dramatically reduces infarct size. Hence, inhibitors of ICAM-1 may provide a novel therapeutic option for acute myocardial infarction.

Key Words: heart • ICAM-1 • acute myocardial infarction




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