Recent advances in understanding of preeclampsia.
Despite intensive research, preeclampsia still accounts for significant morbidity and mortality for the mother and the neonate, especially in developing countries. Recent studies have suggested that excess secretion of a naturally occurring anti-angiogenic molecule of placental origin referred to as soluble fms-like tyrosine kinase-1 (sFlt-1, also referred to as sVEGFR-1) may contribute to the pathogenesis of preeclampsia. sFlt-1 acts by antagonizing two pro-angiogenic molecules - vascular endothelial growth factor (VEGF) and placental growth factor (PlGF). Abnormalities in the angiogenic balance have been proposed as having a major role in the molecular cascade leading to proteinuria, hypertension, and endothelial dysfunction. Further evidence supports the hypothesis that angiogenic balance is crucial to differentiation and invasion of cytotrophoblasts. The abnormal placentation and the accompanying hypoxia may, in turn, result in more sFlt-1 production, thus leading to a vicious cycle of sFlt-1 production, eventually causing preeclampsia. These recent discoveries may facilitate the development of novel strategies for the diagnosis and therapy of preeclampsia.
Bdolah
Yuval
Y
Department of Obstetrics and Gynecology and Reproductive Sciences, Beth Israel Deaconess Medical Center, 330 Brookline Avenue-KS3182, Boston, MA 02215, USA.
Karumanchi
S Ananth
SA
Sachs
Benjamin P
BP
D005260:Female; D006801:Humans; D000860:Hypoxia; D018919:Neovascularization, Physiologic; D010920:Placenta; D000072483:Placenta Growth Factor; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D011257:Pregnancy Proteins; D042461:Vascular Endothelial Growth Factor A
C000608036:PGF protein, human; D011257:Pregnancy Proteins; D042461:Vascular Endothelial Growth Factor A; D000072483:Placenta Growth Factor