From molecules to medicine: a future cure for preeclampsia? Drug News Perspect 2009 Nov;22(9):531-41
Date
01/15/2010Pubmed ID
20072730DOI
10.1358/dnp.2009.22.9.1435464Scopus ID
2-s2.0-76749125403 (requires institutional sign-in at Scopus site) 18 CitationsAbstract
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.
Author List
Santillan MK, Santillan DA, Sigmund CD, Hunter SKAuthor
Curt Sigmund PhD Chair, Professor in the Physiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAntihypertensive Agents
Drug Design
Endothelium, Vascular
Female
Genetic Predisposition to Disease
Humans
Immune System
Oxidative Stress
Phenotype
Placenta
Pre-Eclampsia
Pregnancy
Risk Factors
Signal Transduction