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Inflammation and the pathogenesis of atherosclerosis in systemic lupus erythematosus

David Geffen School of Medicine at The University of California Los Angeles, Division of Rheumatology, Department of Medicine, Los Angeles, California, USA, mmcmahon{at}mednet.ucla.edu

J Grossman

David Geffen School of Medicine at The University of California Los Angeles, Division of Rheumatology, Department of Medicine, Los Angeles, California, USA

W Chen

David Geffen School of Medicine at The University of California Los Angeles, Division of Rheumatology, Department of Medicine, Los Angeles, California, USA

B H Hahn

David Geffen School of Medicine at The University of California Los Angeles, Division of Rheumatology, Department of Medicine, Los Angeles, California, USA

Atherosclerosis is a complicated inflammatory process characterized by the interactions of numerous different moieties including lipids, enzymes, endothelial cells, cytokines, chemokines, leukocytes, adhesion molecules, complement and antibodies. As in the pathogenesis of many lupus disease processes, the increased risk of atherosclerosis seen in systemic lupus erythematosus (SLE) is likely due to the complex interplay of many of these inflammatory mediators. Expanding our understanding of the pathogenesis of atherosclerosis in SLE is critical if we are to improve the quality of care and reduce mortality in this vulnerable population.

Key Words: atherosclerosis • inflammation • oxidized LDL • plaque • SLE

Lupus, Vol. 15, No. 11 suppl, 59-69 (2006)
DOI: 10.1177/0961203306071668


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