The glycation process causes protein damage, and the interaction of AGEs and their receptors could lead to the activation of a number of proinflammatory pathways, increased production of ROS in oocytes, and endothelial dysfunction via inactivation of endothelial nitric oxide synthase and prostacyclin synthase, thereby inducing a premature decline in ovarian function (48, 56). The gene discussed is PTGIS; the disease is endothelial dysfunction.