VEGFA and endothelial dysfunction: A mass of ROS from these sources inactivates biomacromolecules and disrupts cellular metabolism, leading to endothelial dysfunction and excessive trophoblast apoptosis as well as increasing anti-angiogenic soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), which bind and neutralize circulating proangiogenic vascular endothelial growth factor (VEGF) and transforming growth factor-β1 (TGF-β1), respectively [4, 8, 9, 13].