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Preeclampsia: The Role of Angiogenic Factors in Its Pathogenesis
Alice Wang, Sarosh Rana and S. Ananth Karumanchi
Physiology 24:147-158, 2009. ; doi: 10.1152/physiol.00043.2008 You might find this additional info useful... Updated information and services including high resolution figures, can be found at: Additional material andinformation about Physiology can be found at:
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Physiology (formerly published as News in Physiological Science) publishes brief review articles on major physiological developments. It is published bimonthly in February,April, June, August, October, and December by the American Physiological Society, 9650 Rockville Pike, Bethesda MD 20814-3991. Copyright © 2009 the American Physiological Society. ESSN: 1548-9221. Visit our website at

PHYSIOLOGY 24: 147–158, 2009; doi:10.1152/physiol.00043.2008

Alice Wang,1 Sarosh Rana,2 and S. Ananth Karumanchi2–4
1 Division ofNeonatology, Children’s Hospital Boston and Harvard Medical School, Boston; Departments of 2 Obstetrics and Gynecology and 3Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts; and 4Howard Hughes Medical Institute, Chevy Chase, Maryland

Preeclampsia: The Role of Angiogenic Factors in Its Pathogenesis
Preeclampsia, a systemicsyndrome of pregnancy clinically characterized by new onset of proteinuria and hypertension, is associated with significant morbidity and mortality to both mothers and fetuses. The pathogenesis of preeclampsia has been enigmatic; this review will focus on understanding the origins of this disorder. Preeclampsia originates in the placenta, starting with inadequate cytotrophoblast invasion and ending withwidespread maternal endothelial dysfunction. Production of placental anti-angiogenic factors, specifically soluble fms-related tyrosine kinase 1 and soluble endoglin, have

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been shown to be upregulated in preeclampsia. These placental anti-angiogenic factors are released into the maternal circulation; theiractions disrupt the maternal endothelium and result in hypertension, proteinuria, and the other systemic manifestations of preeclampsia. The molecular basis for placental dysregulation of these pathogenic factors remains unknown, remains unknown. Hypoxia is likely an important regulator. Other factors such as alterations in the renin-angiotensin-aldosterone axis, immune maladaption, excessiveshedding of trophoblast debris, oxidative stress, and genetic factors likely contribute to the pathogenesis of the abnormal placentation. As of 2009, the only successful treatment for preeclampsia is delivery. No definitive preventive strategies have been identified. However, several of the recent observations related to phenotypic causality provide stimuli for the development of novel therapies.Preeclampsia, a pregnancy-specific disorder characterized clinically by new onset hypertension and proteinuria after 20 wk of gestation, is the most frequently encountered medical complication during pregnancy, affecting ~3–5% of pregnant women worldwide (108b). In developing countries where access to health care is limited, preeclampsia is a leading cause of maternal mortality, with estimates of>60,000 maternal deaths/yr (108b). In the developed world, the burden of this disease falls on the neonate because of premature deliveries performed to preserve the health of the mother. Worldwide, preeclampsia is associated with a perinatal and neonatal mortality rate of 10% (4). Delivery of the placenta results in resolution of the condition, implicating the placenta as a central culprit in the...
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