MOLECULAR PATHWAYS THAT PLAY A ROLE IN THE PREECLAMPSIA PATHOPHYSIOLOGY

Abstract

Preeclampsia (PE) is an obstetric disease seen in approximately 4-5% of pregnancies progressing with hypertension and urinary proteinuria. It may cause maternal and fetal complications. Despite numerous researches in the field of PE, the underlying pathogenesis remains unclear. However, with these related studies, it has been concluded that there are many molecular mechanisms that trigger PE. Based on these molecular mechanisms, PE can be examined in two stages. The first stage is placental ischemia caused by abnormal placentation. In the second stage, necrotic and apoptotic factors released from the ischemic placenta into the circulation cause systemic inflammation and endothelial dysfunction. One of these factors released from placental cells is the antiangiogenic factor. Also, there is an imbalance in the antioxidant and prooxidant mechanisms that are thought to be due to recurrent ischemia reperfusion injury in PE. The systemic inflammatory response in PE is associated with the immunological response resulting from the contact of the maternal immune cells with trophoblasts. The aim of this review is to present the current molecular mechanisms implicating the pathway leading to PE. The development of new insights into the pathogenesis of PE in conclusion of a better understanding of the relevant molecular mechanisms will guide further studies.