[Circulating endothelial cells, microparticles and progenitors: towards the definition of vascular competence]

Exposure to deleterious processes of metabolic, infectious, autoimmune or mechanical origin, alters the endothelium which progresses towards a proinflammatory and procoagulant activation, senescence and apoptosis. This "response to injury" of the endothelium plays a key role in the initiation and progression of cardiovascular disorders. In the last 10 years, identification in peripheral blood of circulating endothelial cells (CEC) and endothelial-derived microparticles (EMP) reflecting endothelium damage has led to the development of new noninvasive methods for endothelium exploration. Indeed, these biomarkers were associated with most of the cardiovascular risk factors, were correlated with established parameters of endothelial dysfunction, and were indicative of a poor clinical outcome. Moreover, they behave as biological vectors able to disseminate deleterious signals in the vascular compartment. More recently, this concept has been enlarged by the discovery of a potent repair mechanism based on the recruitment of the circulating endothelial progenitors cells (EPC) from the bone marrow, able to regenerate injured endothelial cells. Cardiovascular risk factors alter EPC number and function. Because the damage/repair balance plays a critical role in the endothelium homeostasis, CEC, EMP and EPC could be combined in an endothelium phenotype that defines the "vascular competence" of each individual. In the future, progress in standardization of available methodologies to measure these emerging biomarkers is a crucial step to establish their clinical interest for assessment of vascular risk and monitoring of vascular-directed therapeutics.