Atherosclerosis (AT) and cardiovascular disease (CVD) are enhanced in autoimmune diseases such as antiphospholipid syndrome (APS), systemic lupus erythematosus (SLE), and rheumatoid arthritis (RA). The reason for this accelerated process is still debatable and, although traditional risk factors are more prevalent in those patients than in general population, they do not fully explain that enhanced risk. Inflammatory components of the immune response, mainly interleukins, TNF-α, and IFN-γ, as well as some autoantibodies, including anti-oxidized low density lipoproteins (anti-oxLDL), anti-beta-2-Glycoprotein 1 (anti- β2GPI), anti-Heat shock proteins 60/65 (anti-HSP60/65), and anti-oxLDL/β2GPI have been shown to play a leading role in the pathogenesis of both, AT and CVD. However, the role of the autoantibodies in accelerated AT in autoimmune disease patients is still controversial. Recently, DNA microarray and proteomic-based approaches have made substantial breakthrough into the study of various rheumatic diseases, thus allowing for the discovery of previously unknown proteins involved in CVD including some that may be suitable to be used as biomarkers. Herein, we review recent genomics and proteomic approaches that have been applied to the study of autoimmune diseases with atherosclerotic and CV risk. The pharmacogenomics and pharmacoproteomics studies given over to the analysis of ancient and new drugs used to relieve the physiopathology associated to these complex diseases are also discussed.
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López-Pedrera et al. (2009) studied this question.
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