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Inflammation and atherosclerosis are the major causes of cardiovascular disease (CVD) in SLE. Both traditional and disease-specific risk factors contribute to the formation of endothelial dysfunction. Endothelial progenitor cells (EPCs) have the ability to restore endothelial integrity. The aim of this study was to determine whether the number and function of EPCs are altered in SLE.

Accumulation of VEGFR-2+/CD133+ cells and decreased number and impaired functionality of CD34+/VEGFR-2+ cells in patients with SLE