Then decreased uteroplacental perfusion induces the placenta release excess placental antiangiogenic factor, soluble fms-like tyrosine kinase 1(sFlt1), which antagonizes proangiogenic factors, vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), leading to endothelial dysfunction and systemic vascular dysfunction [32–34]. Here, VEGFA is linked to endothelial dysfunction.