Abstract:
: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.
journal_name
Autoimmunityjournal_title
Autoimmunityauthors
Kaplan MJdoi
10.1080/08916930903002479subject
Has Abstractpub_date
2009-11-01 00:00:00pages
580-6issue
7eissn
0891-6934issn
1607-842Xpii
913562319journal_volume
42pub_type
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