Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized
by the production of autoantibodies against nuclear antigens such as double-stranded
DNA. Lupus predominantly affects women (ratio, 9:1). Moreover, premenopausal women
with SLE are 50 times more likely to have a myocardial infarction. Although specific
risk factors for advanced cardiovascular complications have not been identified in
this patient population, endothelial dysfunction is highly prevalent. Recent studies
show that the type I interferon signature gene expression coincides with impaired
brachial artery flow-mediated dilation and diminished endothelial progenitor cell
circulation, both markers of impaired endothelial function. Although many factors
promote the development of vascular endothelial dysfunction, all pathways converge
on the diminished activity of endothelial nitric oxide synthase (eNOS) and loss of
nitric oxide (NO) bioavailability. Studies examining the effects of type I interferons
on eNOS and NO in SLE are missing. This literature review examines the current literature
regarding the role of type I interferons in cardiovascular disease and its known effects
on regulators of eNOS and NO bioavailability that are important for proper endothelial
cell function.
Key Indexing Terms
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Article info
Publication history
Accepted:
March 21,
2014
Received:
July 29,
2013
Footnotes
Supported by Ralph H. Johnson VA Medical Center (5I01CX00021804), National Institute of Arthritis and Musculoskeletal and Skin Diseases Veterans Affairs Research Enhancement Awards Program (5R01AR04547613), Initiative for Maximizing Student Diversity (IMSD), National Institute of General Medical Sciences National Arthritis Foundation (5R25GM07264308).
The authors have no conflicts of interest to disclose.
Ideas and content presented within this review article have been used as a source to explain unpublished data generated in the Oates laboratory.
Identification
Copyright
© 2014 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.
