Circulation. 2002;106:896-899
doi: 10.1161/01.CIR.0000028962.04520.01
doi: 10.1161/01.CIR.0000028962.04520.01
(Circulation. 2002;106:896.)
© 2002 American Heart Association, Inc.
Editorial |
Platelet-Derived CD40L
The Switch-Hitting Player of Cardiovascular Disease
From Millennium Pharmaceuticals, Inc, South San Francisco, Calif.
Correspondence to David R. Phillips, PhD, Principal Research Scientist, Millennium Pharmaceuticals, Inc, 256 E Grand Ave, South San Francisco, CA 94080. E-mail david.r.phillips@mpi.com
Key Words: Editorials • cardiovascular diseases • platelets • restenosis • glycoproteins
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Studies focusing on cellular and molecular mechanisms that regulate atherosclerosis have fed scientific journals for decades, nearly as long as it takes an atherosclerotic plaque to grow, rupture, and eventually induce vascular occlusive events.
See p 981
Three closely linked lines of research have now merged. In the 1980s, concepts crystallized on the role of lipids (eg, oxidized LDL, elevated cholesterol) in the genesis of atherosclerotic plaque. In the 1990s, use of antiplatelet agents proved that platelet aggregation caused thrombotic ischemic events resulting from the rupture of plaques in advanced lesions and from the vascular injuries inflicted by percutaneous interventions (PCI). Now, atherosclerosis is recognized as an inflammation-mediated disease involving multiple interactions between leukocytes, cells of the vessel wall, and platelets. Indeed, recent studies of predictors of cardiovascular risk rank markers of inflammation (eg, high-sensitive C-reactive protein) as comparable to markers of cholesterol (eg, total cholesterol/HDL cholesterol). Emerging data suggest that CD40L may be at the heart of the atherosclerotic process. What makes CD40L so unique? Its localization and its multifunctionality (Figure 1). CD40L is a surprisingly abundant protein in platelets and may have roles in the inflammatory aspects of atherosclerotic lesion progression, thrombosis, and now, as implied by the work of Urbich et al1 in this issue of Circulation, in restenosis.
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