Secretion of sFLT1 and sENG into the maternal circulation

Abstract

Preeclampsia (PE) is one of the most common diseases worldwide, complicating ~ 5% of all pregnancies. Although no major progress has been achieved in the treatment of PE, our ability to identify women at high-risk has increased considerably during the past decade. Thus, the soluble form of the type-1 receptor of vascular endothelial growth factor (sFlt1) and of endoglin (sEng), an endothelial receptor for transforming growth factor beta, have been shown to increase dramatically in the maternal blood of the women affected some weeks before the onset of clinical symptoms. A relative concomitant fall in VEGF and placental growth factor (PlGF) has also been reported. In 2010, they are the most promising biomarkers for PE. The extent to which they are involved in the pathophysiology of the maternal syndrome and of the primary placental disorder responsible for PE is being actively investigated. In parallel, defective placental steroidogenesis, as well as the loss of tolerance towards the angiotensin-2 receptor have also been found to be critically involved in mouse models of PE. Although there is not much data to support their role in human PE, these two biological pathways are a potential future source of both new biomarkers, and new therapeutic strategies. The aim of this review is to compare the likely value of these molecules at the bedside, and to discuss their implication in the pathophysiology of what used to be known as “the disease of theories”.