sFlt-1 is secreted by the placenta into the maternal circulation and adheres to the receptor-binding domains of placental growth factor and vascular endothelial growth factor (VEGF), preventing interaction with endothelial receptors, blocking VEGF-mediated vasodilation and inducing endothelial dysfunction [8], considered to be key to the pathogenesis of preeclampsia [6]. Here, PGF is linked to endothelial dysfunction.