Abstract:

Pre-eclampsia (PE) is a pregnancy specific syndrome characterized by hypertension and multiple organ dysfunction. Although the specific pathogenesis is not yet clear, insufficient placental perfusion and persistent hypoxia caused by shallow and limited invasion of trophoblasts during placental formation may be important initial events. As an important steroid hormone secreted by the placenta, estrogen regulates target gene expression levels through genomic or non-genomic effects of estrogen receptor (ER) and estrogen response element (ERE) signaling pathways, leading to changes in biological behaviors such as trophoblast proliferation, apoptosis, invasion, and possibly mediating the loss of endometrial decidualization, thereby participating in placental shallow implantation and the occurrence of insufficient perfusion. Estrogen and its signaling pathways can also regulate the levels of vasoactive factors such as nitric oxide and the activity of related ion channels to regulate the contractile and relaxing ability of uterine artery smooth muscle, and participate in the occurrence and development of high-risk pregnancies such as PE and recurrent spontaneous abortion through various mechanisms.

Key words: Pre-eclampsia, Estrogens, Receptors, estrogen, Signaling pathway, Pathogenesis