Abstract
Preeclampsia is a prevalent disorder that remains one of the more frequent sources of morbidity and mortality for pregnant women and their children. There is evidence that fetuses and newborns of preeclamptic women (NPW) are specifically affected by the maternal condition, independent of the uteroplacental flow restriction. Preeclampsia is thought to be an endothelial disorder in which pathophysiological oxidative stress plays an important role. Experimental and clinical studies suggest that maternal endothelial dysfunction and oxidative stress correlate with the severity of complications for NPW. In this regard, the fetus seems not to be a passive spectator suffering from the maternal condition, as fetal vasculature somehow shares the particular endothelial dysfunction; this has been demonstrated in umbilical vessels and endothelial cells from NPW, and in fetal systemic vessels in animal models of preeclampsia. In addition, oxidative stress is increased in fetal circulation in preeclampsia. Maternal symptoms disappear soon after delivery, supporting the critical role of the placenta in this disorder. There is growing evidence to suggest that the placenta could be the source of some factor(s) impairing endothelial function, both in preeclamptic women and their fetuses. Whether oxidative stress is a cause or a consequence of the dysfunction is a matter of controversy. In any case, this unfavorable milieu might imprint fetal vasculature, increasing the risk of future vascular disorders in NPW.
Financial disclosure
The authors have no relevant financial interests related to this manuscript, including employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.