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.
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