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Cardiovascular Research 2006 69(2):341-347; doi:10.1016/j.cardiores.2005.09.018
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Copyright © 2005, European Society of Cardiology

Mycophenolate mofetil (MMF): Firing at the atherosclerotic plaque from different angles?

Sander I. van Leuvena, John J.P. Kasteleina, Anthony C. Allisonb, Michael R. Haydenc and Erik S.G. Stroesa,*

aDepartment of Vascular Medicine, Academic Medical Center, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands
bAlavita Corporation, Menlo Park, California, USA
cCentre for Molecular Medicine and Therapeutics, Department of Medical Genetics, University of British Columbia, Vancouver, Canada

* Corresponding author. Fax: +31 20 5669343. Email address: e.s.stroes{at}amc.uva.nl

Atherosclerosis is characterized by a persistent, low-grade inflammatory state in which immune cell activation is inseparably linked to plaque formation and destabilization. The T-lymphocyte in particular has emerged as a pivotal player throughout the course of atherogenesis. As a consequence, the concept that immune modulation is a suitable target for cardiovascular prevention is currently an important focus of research.

Mycophenolate mofetil (MMF) has emerged as a non-competitive inhibitor of inosine monophosphate dehydrogenase (IMPDH) that exerts cytostatic effects, particularly on proliferating T-lymphocytes. In addition, MMF has other immune-modulating effects, such as downregulation of the expression of adhesion molecules and attenuation of monocyte and macrophage responses. Given the added benefit that MMF is well tolerated, this immunosuppressive agent constitutes an attractive candidate for the modulation of inflammatory activation in atherogenesis. The present review provides an overview of the potential anti-atherogenic properties of MMF.

KEYWORDS Atherosclerosis; Mycophenolate mofetil; Leukocytes; Endothelium; Adhesion molecules

Time for primary review 30 days


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