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The risk of cardiovascular disease is five- to 10-fold increased in most autoimmune disorders1 and adjustment for classical atherogenic factors cannot fully explain it.2 In contrast to the classical view of the endothelium as an inert lining for blood vessels, recent publications suggest a continuous turnover of endothelial cells (ECs), replaced by endotheliocytes adjacent to the lesions or mobilised from the bone marrow (haematopoietic stem cells (HSCs); these display both a haematopoietic and an endothelial differentiating potential and throughout the endothelial lineage are transformed into so-called endothelial progenitor cells (EPCs).3 Patients with systemic lupus erythematosus (SLE) show progenitor depletion, even during clinical remission, caused by increased HSC apoptosis,4 indicating that endogenous vascular repair is impaired and …
Competing interests: None declared.
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