Endothelial microparticles and arterial stiffness: casual coincidence or causative culprit?

I t is widely believed that cardiovascular risk factors promote atherogenesis by damaging endothelium. Endothelial status has been mainly assessed by focusing the attention on the quantification of the endothelium capacity to modulate arterial vasomotion. An alternative way to get information on endothelial health is to measure products of endothelial cell injury. Quantification of circulating endothelial cells has been suggested as a method of assessing endothelial damage, given that exposure of the endothelium to most cardiovascular risk factors may cause the detachment of endothelial cells from the intimal monolayer, thus releasing mature endothelial cells in peripheral blood. More recently, there has been considerable interest in a novel marker of endothelial cell injury, namely endothelial microparticles (EMPs). Microparticles are small vesicles released from the membrane surface during cell activation, injury, or apoptosis, and display the typical surface cell proteins and cytoplasmic components of their cell origin. Endothelial cell vesiculation happens also under physiologic condition, possibly as a mechanism of endothelial cell renewal or cross-talk with other cellular targets. Elevated levels of EMPs, mostly defined as CD31 /CD42 MPs, are found in patients with a variety of vascular diseases and in subjects exposed to cardiovascular risk factors. In the setting of hypercholesterolemia, we had previously found that the number of circulating CD31 /CD42 microparticles was associated with aortic stiffness and that microparticles from hypercholesterolemic patients cause a significant impairment of endothelial repair in vitro. In this issue of the Journal, Wang et al explored the association between EMPs and systemic arterial stiffness in healthy humans. They found that the number of