For more than half a century “treating” hypertension to prolong pregnancy for better fetal maturity has been the core of managing preeclampsia. The recognition, most effectively forwarded by Jim Roberts and Chris Redman more than 20 years ago, that maternal endothelial dysfunction secondary to placental “factors” fundamentally underlies the maternal features of preeclampsia heralded opportunities for new approaches to management. Since that time our understanding of the vasoactive “factors” released by the placenta and the endothelial cell pathways disturbed by those factors have advanced significantly. Indeed, the field is now poised for significant new treatment strategies, for both placental and endothelial cell targets, such that a secondary “cure” for preeclampsia is, at last, a genuine prospect.
We have identified pathways within the endothelial cell (EC) that offer promise of targeted therapies at different points. Using our example of activin-NADP(H) oxidase-EC dysfunction, examples of novel therapeutic targets will be discussed and explored, including optimising cellular anti-oxidant therapy and stabilising EC function. The importance of animal models of preeclampsia in informing best design for clinical interventions will also be explored, emphasising the critical role of experimental research in advancing what is a uniquely a clinical human disease.