Oxidative stress in pre-eclampsia; have we been looking in the wrong place?

Abstract

Pre-eclampsia is a disorder of late pregnancy. It is a major cause of maternal and perinatal morbidity and mortality, accounting for nearly 18% of all maternal deaths worldwide; an estimated 77,000 maternal deaths per year [1]. Poor placentation is considered to be an initial cause of the placental ischemia [2]. Placental ischemia in turn gives rise to oxidative stress in the placenta and leads to shedding of syncytiotrophoblast debris into the maternal circulation provoking a systemic maternal inflammatory response and release of sFLT and sENG causing maternal vascular endothelial dysfunction. The ubiquitous nature of the maternal vascular endothelium accounts for the diverse multi-system nature of pre-eclampsia. Currently there is no treatment for pre-eclampsia except delivery of the placenta and the baby, with the attendant risk of iatrogenic prematurity and significant neonatal morbidity and mortality. As a result, intensive research endeavours have focused on defining the molecular mechanisms of pre-eclampsia and the identification of new pre-symptomatic biomarkers of the condition. This review focuses on the role of elevated oxidative stress in the pathology of pre-eclampsia and potential therapeutic agents targeting oxidative stress that may prevent or ameliorate this disorder.