• Joy N Jones Buie and Jim C Oates.
• Division of Rheumatology and Immunology in the Department of Medicine, Medical University of South Carolina; and Division of Rheumatology and Immunology (JNJB, JCO), Department of Microbiology and Immunology, Medical Research Service of the Ralph H. Johnson VAMC, The Medical University of South Carolina, Charleston, South Carolina.
• Am. J. Med. Sci. 2014 Aug 1; 348 (2): 168175168-75.

AbstractSystemic 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.

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