Fetoplacental Vascular Endothelial Dysfunction as an Early Phenomenon in the Programming of Human Adult Diseases in Subjects Born from Gestational Diabetes Mellitus or Obesity in Pregnancy
Figure 5
Potential pathophysiological interaction between the mother, the placenta, and the fetus in fetal atherosclerosis. Maternal factors, including reduced (ā) catalase (CAT) activity, increased (ā) lipid peroxidation, and oxidized low density lipoproteins (oxLDL), associated with increased cholesterol content at the mother circulation, generate a state of maternal supraphysiological hypercholesterolaemia (MSPH). This phenomenon leads to similar alterations in the placenta (reduced CAT, superoxide dismutase (SOD), glutathione-peroxidase (GSH-Px) activity) and the fetus (with reduced CAT and GSH-Px and increased lipid peroxidation and oxLDL). Therefore, atherosclerosis in the fetus is identified. Data taken from [88, 100, 101, 109, 110].
