Figure 2.

Mechanism of PE Pathogenesis. Placental ischemia induces AT1 autoantibody formation, which further increases Ang-II sensitivity, leading to enhanced ET-1, sFlt-1, and ROS production. sFlt-1 acts as a decoy receptor and blocks free VEGF to protect the fetus from toxicity by excess VEGF, although there is endothelial dysfunction and effect on kidney. AT1 = Angiotensin-II type 1, Ang-II = angiotensin-II, ET-1 = Endothelin-1, sFlt-1 = soluble fms-like tyrosine kinase-1, ROS = Reactive Oxygen Species, VEGF = Vascular Endothelial Growth Factor, KDR = Kinase insert Domain Receptor and sEng=soluble endoglin.