Document Detail


The role of hypoxia and hypoxia-inducible factor-1alpha in preeclampsia pathogenesis.
MedLine Citation:
PMID:  23034156     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Preeclampsia affects 5%-8% of pregnancies and is the leading worldwide cause of maternal and fetal morbidity and mortality. Preeclampsia is associated with shallow trophoblast invasion and inadequate spiral artery remodeling, which are widely believed to lead to placental hypoxia, the putative culprit initiating the cascade of events that ultimately results in the maternal manifestations of the disease. Despite extensive research, however, the pathophysiology of this disease remains poorly understood, no effective prevention exists, and treatment is limited to symptomatic therapy. Recent research has introduced exciting new theories regarding the pathogenesis of preeclampsia. Clinical and experimental evidence implicating the circulating antiangiogenic molecules soluble Fms-like tyrosine kinase-1 (sFLT-1) and soluble endoglin (sENG), as well as endothelin-1 and the angiotensin II receptor type I autoimmune antibody (AT-1AA), have been especially promising. This review collates evidence for a role of hypoxia and hypoxia-inducible factor-1alpha (HIF1A; referred to as HIF-1α throughout) in the pathogenesis of preeclampsia and discusses possible molecular links between hypoxia and the newly reported potential mediators of the disease's manifestations.
Authors:
Reshef Tal
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Publication Detail:
Type:  Journal Article; Review     Date:  2012-12-13
Journal Detail:
Title:  Biology of reproduction     Volume:  87     ISSN:  1529-7268     ISO Abbreviation:  Biol. Reprod.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-12-17     Completed Date:  2013-05-14     Revised Date:  2013-06-17    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  United States    
Other Details:
Languages:  eng     Pagination:  134     Citation Subset:  IM    
Affiliation:
Department of Obstetrics and Gynecology, Maimonides Medical Center, Brooklyn, New York 11219, USA. resheft@gmail.com
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD / blood,  chemistry,  metabolism
Autoantibodies / analysis
Cell Hypoxia*
Endothelin-1 / blood,  chemistry,  metabolism
Female
Humans
Hypoxia-Inducible Factor 1, alpha Subunit / antagonists & inhibitors,  biosynthesis,  metabolism*
Placenta / immunology,  metabolism*
Pre-Eclampsia / blood,  etiology*,  immunology,  metabolism
Pregnancy
Receptor, Angiotensin, Type 1 / chemistry
Receptors, Cell Surface / blood,  chemistry,  metabolism
Solubility
Vascular Endothelial Growth Factor Receptor-1 / blood,  chemistry,  metabolism
Chemical
Reg. No./Substance:
0/AGTR1 protein, human; 0/Antigens, CD; 0/Autoantibodies; 0/ENG protein, human; 0/Endothelin-1; 0/HIF1A protein, human; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 0/Receptor, Angiotensin, Type 1; 0/Receptors, Cell Surface; EC 2.7.10.1/FLT1 protein, human; EC 2.7.10.1/Vascular Endothelial Growth Factor Receptor-1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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