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Inflammation in early atherogenesis: impact of ACE inhibition

R. De Caterina*,1,2 and C. Manes3

a "G. d'Annunzio" University, Chieti, Italy
b CNR Institute of Clinical Physiology, Pisa, Italy
c Institute of Cardiology, Bologna University, Italy

* Raffaele De Caterina, MD, PhD, Chair of Cardiology, "G. d'Annunzio" University - Chieti, c/o Ospedale S. Camillo de Lellis, Via Forlanini, 50, 66100 Chieti, Italy.

Abstract

Cytokines and other inflammatory mediators induce functional changes in the endothelium ("endothelium activation"), which have been shown to be markers of atherosclerotic vascular disease. Endothelial activation accompanies and promotes vascular disease, and is associated with overexpression of chemoattractants and adhesion molecules, which in turn lead to leukocyte binding to the endothelium. The nuclear factor-{kappa}B (NF-{kappa}B) system appears to regulate the expression of many of the genes involved in this process. Angiotensin II contributes to atherogenesis by increasing expression of many pro-inflammatory genes, in part by inducing oxidative stress, which activates NF-{kappa}B.

Key Words: ACE inhibitors • oxidative stress • inflammation


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