Journal
MICROVASCULAR RESEARCH
Volume 75, Issue 1, Pages 1-8Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mvr.2007.04.009
Keywords
preeclampsia; angiogenesis; soluble fms-like tyrosine kinase-1; sFlt-1; vascular endothelial growth factor; VEGF; placental growth factor; PlGF; hypoxia; placenta; pregnancy; hypertension; proteinuria; endoglin; sEng
Categories
Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL079594] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK065997] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL079594, R01 HL079594-03, R01 HL 079594] Funding Source: Medline
- NIDDK NIH HHS [R01 DK065997-04, R01 DK065997, R01 DK 065997] Funding Source: Medline
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Preeclampsia is a major cause of maternal, fetal and neonatal mortality worldwide. The mechanisms that initiate preeclampsia in humans have been elusive, but some parts of the puzzle have begun to come together. A key discovery in the field was the realization that its major phenotypes, such as hypertension and proteinuria, are due to excess circulating soluble fins-like tyrosine kinase-1 (sFlt-1, also referred to as sVEGFR-1). sFlt-1 is an endogenous anti-angiogenic protein that is made by the placenta and acts by neutralizing the pro-angiogenic proteins vascular endothelial growth factor (VEGF) and placental growth factor (PIGF). More recently, soluble endoglin, another circulating anti-angiogenic protein was found to synergize with sFlt-1 and contribute to the pathogenesis of preeclampsia. Abnormalities in these circulating angiogenic proteins are not only present during clinical preeclampsia, but also antedate clinical symptoms by several weeks. This review will summarize our current understanding of the molecular mechanism of preeclampsia, with an emphasis on the recently characterized circulating anti-angiogenic proteins. (c) 2007 Elsevier Inc. All rights reserved.
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