Preeclampsia affects 5-10% of pregnancies and is responsible for substantial maternal and neonatal morbidity and mortality. It is believed to be a two-stage disease with an initial placental trigger with no maternal symptoms followed by a maternal syndrome characterized by hypertension, proteinuria, and endothelial dysfunction. The first stage is thought to be due to shallow cytotrophoblast invasion of maternal spiral arterioles leading to placental insufficiency. The diseased placenta in turn releases soluble angiogenic factors that induce systemic endothelial dysfunction and clinical preeclampsia during the second stage. This review will discuss the role of circulating angiogenic factors of placental origin as potential mediators of the systemic endothelial dysfunction and the clinical syndrome of preeclampsia and provide an evolutionary explanation for this phenomenon.
Yuan, Hai-TaoHaig, DavidAnanth Karumanchi, SengDK 065997/DK/NIDDK NIH HHS/HL079594/HL/NHLBI NIH HHS/Research Support, N.I.H., ExtramuralReview2005/12/14 09:00Curr Top Dev Biol. 2005;71:297-312.