HIF1A and endothelial dysfunction: Endothelial dysfunction after prenatal hypoxia develops against a background of HIF-1α deficiency (a factor that activates eNOS expression through serine residue phosphorylation) and nitrosative stress, which also leads to HSP70 deficiency, glutathione system depletion, reduced NO bioavailability, and suppression of gene transcription by cytotoxic NO products [12,16,25].