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REVIEW

Preeclampsia: The Role of Angiogenic Factors in Its Pathogenesis

Alice Wang¹, Sarosh Rana² and S. Ananth Karumanchi^2,3,4

¹ Division of Neonatology, Children’s Hospital Boston and Harvard Medical School, Boston;
² Departments of Obstetrics and Gynecology and
³ Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts; and
⁴ Howard Hughes Medical Institute, Chevy Chase, Maryland sananth{at}bidmc.harvard.edu

Preeclampsia, a systemic syndrome 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 with widespread maternal endothelial dysfunction. Production of placental anti-angiogenic factors, specifically soluble fms-related tyrosine kinase 1 and soluble endoglin, have been shown to be upregulated in preeclampsia. These placental anti-angiogenic factors are released into the maternal circulation; their actions 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, excessive shedding 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.

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