Document Detail


From molecules to medicine: a future cure for preeclampsia?
MedLine Citation:
PMID:  20072730     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the United States, preeclampsia (PreE) affects 5-7% of all pregnancies, yet represents 15% of all maternal-fetal morbidity and mortality. PreE causes fetal growth restriction, oligohydramnios, fetal death, and maternal seizures, stroke, cerebrovascular hemorrhage and death. It has immediate and potentially long-term effects on both the fetus and mother. To date, the molecular pathogenesis of PreE is largely unknown. Multiple pathways, including dysfunctional angiogenesis, inappropriate placentation, oxidative stress and an altered immunological milieu have been proposed as key players in the development of PreE. In addition, genetic factors in all of these pathways are essential components in the etiology of this disease. This review introduces the clinical presentation of PreE and its particular disease phenotype that has prompted some of the molecular investigations of its etiology. Evidence of the many molecular pathways involved in the pathogenesis of PreE, as well as the therapeutic investigations targeting these pathways, is presented.
Authors:
Mark K Santillan; Donna A Santillan; Curt D Sigmund; Stephen K Hunter
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Drug news & perspectives     Volume:  22     ISSN:  0214-0934     ISO Abbreviation:  Drug News Perspect.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2010-01-14     Completed Date:  2010-03-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8809164     Medline TA:  Drug News Perspect     Country:  Spain    
Other Details:
Languages:  eng     Pagination:  531-41     Citation Subset:  IM    
Copyright Information:
Copyright 2009 Prous Science, S.A.U. or its licensors. All rights reserved.
Affiliation:
Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, University of Iowa Hospitals and Clinics, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa, USA. mark-santillan@uiowa.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Antihypertensive Agents / chemistry,  pharmacology,  therapeutic use*
Drug Design*
Endothelium, Vascular / drug effects,  physiopathology
Female
Genetic Predisposition to Disease
Humans
Immune System / drug effects,  physiopathology
Oxidative Stress
Phenotype
Placenta / drug effects,  physiopathology
Pre-Eclampsia / drug therapy*,  etiology,  physiopathology
Pregnancy
Risk Factors
Signal Transduction / drug effects*
Grant Support
ID/Acronym/Agency:
5-KL2-RR024980-2/RR/NCRR NIH HHS; 5-UL-1RR024979-2/RR/NCRR NIH HHS; AI-07260-22/AI/NIAID NIH HHS; P01 HL084207/HL/NHLBI NIH HHS; T32 HL1007121/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antihypertensive Agents

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


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