Angiogenic Factors in Preeclampsia From Diagnosis to Therapy

During the past decade, epidemiological, experimental, and therapeutic studies have provided evidence that altered antiangiogenic state because of altered circulating sFlt1 and related proteins, such as PlGF and sEng leads to preeclampsia.109 Recent study suggests that sFlt1 and sEng are largely expressed in syncytial knots in the placenta and released into maternal circulation as syncytial microparticles.42 Understanding the dysregulated antiangiogenic pathway in the syncytium and its role in mediating maternal vascular disease marks a significant advance in our efforts to explain the origins of preeclampsia. Further study on the basic biology of placentation and syncytialization may shed clues on fundamental molecular defect in preeclampsia. Several clinical studies have demonstrated a potential role for the use of angiogenic biomarkers for aid in the diagnosis and prognosis of preterm preeclampsia. We now need clinical trials demonstrating the use of these biomarkers in helping obstetrician's management decisions, improve health outcomes or reduce costs to the healthcare system. Targeted therapies against angiogenic pathway are promising; however, only time will prove whether they will be effective. After decades of modest progress, in the past few years, the field has witnessed remarkable successes with the use of biomarkers and the development of therapies targeting specific molecular pathways and have brought hope to numerous women worldwide. In addition, we speculate that exposure to antiangiogenic factors during preeclampsia may lead to longterm changes to the vasculature that can have adverse consequences to maternal health. © 2016 American Heart Association, Inc.