Premature vascular damage in systemic lupus erythematosus.
Systemic lupus erythematosus (SLE) is a disease associated with a striking increase in the risk of premature cardiovascular (CV) complications due to accelerated atherosclerosis. Traditional CV risk factors seem to be less important predictors of CV events than the presence of active SLE. Immune dysregulation characteristic of lupus appears to play the dominant role in atherogenesis. While both SLE-specific and non-specific mechanisms have been proposed to play a prominent role in the induction of premature vascular damage in this disease, the exact etiology remains unclear. We have proposed that an imbalance between vascular damage and repair likely induced by Interferon- could play a prominent role in the induction of accelerated atherosclerosis in SLE. This review summarizes some of the proposed mechanisms that may promote accelerated vascular damage in lupus and explores potential targets for CV risk prevention in this patient population.
Kaplan
Mariana J
MJ
Division of Rheumatology, Department of Internal Medicine and Graduate Program in Immunology, University of Michigan Medical School, Ann Arbor, MI 48109-5680, USA. makaplan@umich.edu
D000818:Animals; D017209:Apoptosis / Q000276:immunology; D001323:Autoantibodies / Q000097:blood; D001808:Blood Vessels / Q000276:immunology*; D002318:Cardiovascular Diseases / Q000276:immunology* / Q000517:prevention & control; D006801:Humans; D007370:Interferon Type I / Q000276:immunology / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000276:immunology*; D042461:Vascular Endothelial Growth Factor A / Q000276:immunology / Q000378:metabolism
D001323:Autoantibodies; D007370:Interferon Type I; D042461:Vascular Endothelial Growth Factor A