Angiogenic factors and preeclampsia

Abstract

Introduction Preeclampsia is a systemic syndrome of pregnancy, which is characterized by widespread maternal endothelial dysfunction [1]. It is a leading cause of maternal and neonatal morbidity and mortality, affecting between 3% and 5% of all pregnancies in the developed world [2]. Symptoms of preeclampsia include de novo hypertension and proteinuria usually after 20 weeks of gestation. Although the exact molecular pathogenesis of preeclampsia is largely unknown, it is widely accepted that placental dysfunction is a major factor in the development of preeclampsia. The placenta plays a key pathogenic role in preeclampsia based on two observations. First, to date the only effective treatment of preeclampsia is removal of the placenta. Women suffering from preeclampsia often see their symptoms resolve within 24 to 48 hours of delivery. Second, women with a molar pregnancy, in which there is hyperplastic growth of the placenta in the absence of a fetus, may be affected by preeclampsia. These patients may develop severe early onset preeclampsia and the symptoms usually resolve when the molar tissue is removed [3, 4]. More recently, studies have shown that an imbalance in the secretion of placenta-associated angiogenic proteins contributes to the pathogenesis of the disease. These proteins include the antiangiogenic factors soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin. This chapter will focus on the emerging role of angiogenic and antiangiogenic factors in the pathogenesis of preeclampsia and how these factors may play an important role in mediating the clinical features of the disease.