The state of placental insufficiency triggers an imbalance in the placental release of angiogenesis regulatory factors to the maternal circulation, characterized by decreased concentrations of proangiogenic factors such as placental growth factor (PlGF) and elevated concentrations of prohypertensive and antiangiogenic factors such as soluble fms-like tyrosine kinase-1 (sFlt-1) [16, 17]. Here, PGF is linked to placental insufficiency.