on March 8, 2004
Published online before print March 8, 2004, doi: 10.1161/01.HYP.0000123070.31763.55
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Submitted on October 29, 2003
From the Department of Molecular and Cellular Physiology (D.N.G.), Louisiana State University Health Sciences Center, Shreveport; the Department of General Surgery (T.V.), University of Münster, Germany; and the University Clinic for Pediatric Surgery (T.P.), University of Graz, Austria. * To whom correspondence should be addressed. E-mail: dgrang{at}lsuhsc.edu.
Abstract--There is a growing body of evidence that inflammation might play an important role in the initiation and progression of cardiovascular diseases (CVDs). The designation of CVD as a chronic inflammatory process is further supported by evidence that the risk factors for CVD cause endothelial cells throughout the vascular tree to assume an inflammatory phenotype. These activated endothelial cells characteristically exhibit oxidative stress and increased adhesiveness for circulating leukocytes. Although initial efforts to define the mechanisms underlying the inflammatory phenotype in diseased endothelial cells have focused on the linkage between oxidative stress and adhesion molecule activation/expression, recent work has implicated a variety of additional factors that can modulate the magnitude and/or nature of the inflammatory responses in CVD. Platelets, angiotensin II, and the CD40/CD40 ligand signaling system are gaining recognition as contributors to the pathogenesis of CVD. These factors appear to converge with known pathways that link oxidative stress with adhesion molecule expression and help to explain the apparent integration of coagulation with inflammation in CVD. These factors also hold the promise of offering multiple sites for therapeutic intervention in CVD.
Revised on December 17, 2003
Modulation of the Inflammatory Response in Cardiovascular Disease
D. Neil Granger*;
Key words: oxidative stress • integrins • angiotensin II • adhesion molecules
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