Abstract
Patients with systemic lupus erythematosus (SLE) have a greatly increased risk of cardiovascular disease. There is growing interest in the link between vascular damage and lupus-specific inflammatory factors. Impaired endothelial repair could account for the endothelial dysfunction in this patient group. This review describes the contribution that endothelial progenitor cells could play in the pathogenesis of premature vascular damage in this disease. The methods of isolation, detection, and characterization of endothelial progenitor cells, together with their potential role in repair of the endothelium and as a therapeutic target in SLE, are discussed.
Highlights
Patients with systemic lupus erythematosus (SLE) have a greatly increased risk of cardiovascular disease
The vascular endothelium is the largest organ of the body and comprises a highly dynamic single layer of endothelial cells (ECs) that are pivotal in the regulation of vascular tone and that have
Modulation of endothelial progenitor cell (EPC) numbers has been identified with cardiovascular disease or vascular trauma, there is still much controversy regarding their true identity and role [7]
Summary
Patients with systemic lupus erythematosus (SLE) have a greatly increased risk of cardiovascular disease. Cardiovascular disease, endothelial progenitor cells, and systemic lupus erythematosus Over the past decade, quantitative analysis of EPCs by using both flow cytometry or cell culture experiments or both has shown that EPC numbers vary in relation to cardiovascular risk factors and atherosclerotic disease in the general population [7,48], and more recently these findings have been extended to patients with SLE (Table 1).
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