Variants in the fetal genome near FLT1 are associated with risk of preeclampsia
Author:
Publisher
Springer Science and Business Media LLC
Subject
Genetics
Link
http://www.nature.com/articles/ng.3895.pdf
Reference30 articles.
1. Souza, J.P. et al. Moving beyond essential interventions for reduction of maternal mortality (the WHO Multicountry Survey on Maternal and Newborn Health): a cross-sectional study. Lancet 381, 1747–1755 (2013).
2. Cnattingius, S., Reilly, M., Pawitan, Y. & Lichtenstein, P. Maternal and fetal genetic factors account for most of familial aggregation of preeclampsia: a population-based Swedish cohort study. Am. J. Med. Genet. A. 130A, 365–371 (2004).
3. Johnson, M.P. et al. Genome-wide association scan identifies a risk locus for preeclampsia on 2q14, near the inhibin, beta B gene. PLoS One 7, e33666 (2012).
4. Zhao, L. et al. Genome-wide association study identifies a maternal copy-number deletion in PSG11 enriched among preeclampsia patients. BMC Pregnancy Childbirth 12, 61 (2012).
5. Maynard, S.E. et al. Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. J. Clin. Invest. 111, 649–658 (2003).
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