TY - JOUR
T1 - New insights into the genetics of preeclampsia
AU - Morgan, T.
AU - Ward, K.
N1 - Funding Information:
From the Departments of Human Genetics and Obstetrics and Gynecology, University of Utah Health Sciences Center, Salt Lake City, UT This work was supported by a grant from The Willard L. Eccles Charitable Trust, the March of Dimes (#6-FY95-0193), and from the National Institutes of Health (1RO1-HD 32170-01j Address reprint requests to KennethW ard, MD, Eccles Institute of Human Genetics, Room 2420, 2030East lO North, Salt Lake City, Utah 84112. Copyright 9 1999 by W..B. Saunders Company O146-0005/99/2301-0003510. 00/0
PY - 1999
Y1 - 1999
N2 - Preeclampsia is familial. Pedigree analyses suggest that one or more common alleles may act as 'preeclampsia susceptibility genes.' The authors speculate that genes involved in blood pressure control, volume regulation, placental health, vascular disease, and vascular remodeling, underlie familial susceptibility to preeclampsia. Several candidate genes have been examined. These data suggest that a common mutation in the angiotensinogen promoter, A(-6), leads to elevated expression of this gene and pleiotropic effects, including abnormal spiral artery remodeling and failed hypervolemia of pregnancy. The factor V Leiden mutation, which predisposes women to thromboembolic disorders during pregnancy, has been implicated as another preeclampsia susceptibility gene. New insights into the genetics of preeclampsia will contribute to the understanding of this disease and should ultimately lead to improved diagnosis and treatment.
AB - Preeclampsia is familial. Pedigree analyses suggest that one or more common alleles may act as 'preeclampsia susceptibility genes.' The authors speculate that genes involved in blood pressure control, volume regulation, placental health, vascular disease, and vascular remodeling, underlie familial susceptibility to preeclampsia. Several candidate genes have been examined. These data suggest that a common mutation in the angiotensinogen promoter, A(-6), leads to elevated expression of this gene and pleiotropic effects, including abnormal spiral artery remodeling and failed hypervolemia of pregnancy. The factor V Leiden mutation, which predisposes women to thromboembolic disorders during pregnancy, has been implicated as another preeclampsia susceptibility gene. New insights into the genetics of preeclampsia will contribute to the understanding of this disease and should ultimately lead to improved diagnosis and treatment.
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U2 - 10.1016/S0146-0005(99)80056-1
DO - 10.1016/S0146-0005(99)80056-1
M3 - Article
C2 - 10102167
AN - SCOPUS:0033041759
SN - 0146-0005
VL - 23
SP - 14
EP - 23
JO - Seminars in Perinatology
JF - Seminars in Perinatology
IS - 1
ER -