The maternal syndrome of preeclampsia is mediated by dysfunctional syncytiotrophoblast
(STB). When this is stressed by uteroplacental malperfusion, its signaling to the mother
changes, as part of a highly coordinated stress response. The STB signals are both
proinflammatory and dysangiogenic such that the preeclamptic mother has a stronger
vascular inflammatory response than normal, with an antiangiogenic bias. Angiogenic
factors have limitations as preeclampsia biomarkers, especially for prediction and diagnosis …