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Rheumatology Advance Access originally published online on October 16, 2008
Rheumatology 2009 48(1):11-22; doi:10.1093/rheumatology/ken395
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

REVIEWS

Common inflammatory mediators orchestrate pathophysiological processes in rheumatoid arthritis and atherosclerosis

F. Montecucco1 and F. Mach1

1Division of Cardiology, Department of Medicine, Geneva University Hospital, Foundation for Medical Researches, Geneva, Switzerland.

Correspondence to: F. Mach, Division of Cardiology, Department of Medicine, Geneva University Hospital, Foundation for Medical Researches, 64 Avenue Roseraie, 1211 Geneva, Switzerland. E-mail: Francois.Mach{at}medecine.unige.ch


  Abstract

RA is characterized by a systemic inflammatory state, in which immune cells and soluble mediators play a crucial role. These inflammatory processes resemble those in other chronic inflammatory diseases, such as atherosclerosis. The chronic systemic inflammation in RA can be considered as an independent risk factor for the development of atherosclerosis, and represents an important field to investigate the reasons of the increase of acute cardiovascular events in RA. In the present review, we focused on several mediators of autoimmunity, inflammation and endothelial dysfunction, which can be considered the most promising targets to prevent atherogenesis in RA. Among several mediators, the pro-inflammatory cytokine TNF-{alpha} has been shown as a crucial factor to induce atherosclerosis in RA patients.

KEY WORDS: Rheumatoid arthritis, Cardiovascular, Cytokine and inflammatory mediators, Inflammation, Chemotactic factors

Submitted 20 May 2008; revised version accepted 10 September 2008.
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