Molecular Mechanisms of Preeclampsia

  1. S. Ananth Karumanchi1,3
  1. 1Department of Medicine, Obstetrics & Gynecology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02214
  2. 2Gulbenkian Program for Advanced Medical Education, 1067-001 Lisbon, Portugal
  3. 3Howard Hughes Medical Institute, Chevy Chase, Maryland 20815
  1. Correspondence: sananth{at}bidmc.harvard.edu

Abstract

Preeclampsia is a pregnancy-specific disease characterized by new onset hypertension and proteinuria after 20 wk of gestation. It is a leading cause of maternal and fetal morbidity and mortality worldwide. Exciting discoveries in the last decade have contributed to a better understanding of the molecular basis of this disease. Epidemiological, experimental, and therapeutic studies from several laboratories have provided compelling evidence that an antiangiogenic state owing to alterations in circulating angiogenic factors leads to preeclampsia. In this review, we highlight the role of key circulating antiangiogenic factors as pathogenic biomarkers and in the development of novel therapies for preeclampsia.

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