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Science 10 June 2005:
Vol. 308. no. 5728, pp. 1592 - 1594
DOI: 10.1126/science.1111726
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Review

Latest Advances in Understanding Preeclampsia

Christopher W. Redman* and Ian L. Sargent

Preeclampsia is a relatively common pregnancy disorder that originates in the placenta and causes variable maternal and fetal problems. In the worst cases, it may threaten the survival of both mother and baby. We summarize recent work on the causes of preeclampsia, which reveals a new mode of maternal immune recognition of the fetus, relevant to the condition. The circulating factors derived from the placenta, which contributes to the clinical syndrome, are now better understood. This brief review on preeclampsia does not cover all aspects of this intriguing condition but focuses on some new and interesting findings.

Nuffield Department of Obstetrics and Gynaecology, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.

* To whom correspondence should be addressed. E-mail: christopher.redman{at}obs-gyn.ox.ac.uk

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Dysregulation of the Circulating and Tissue-Based Renin-Angiotensin System in Preeclampsia.
F. Herse, R. Dechend, N. K. Harsem, G. Wallukat, J. Janke, F. Qadri, L. Hering, D. N. Muller, F. C. Luft, and A. C. Staff (2007)
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Clin. Chem. 53, 42-52
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Expressional and Epigenetic Alterations of Placental Serine Protease Inhibitors: SERPINA3 Is a Potential Marker of Preeclampsia.
S. T. Chelbi, F. Mondon, H. Jammes, C. Buffat, T.-M. Mignot, J. Tost, F. Busato, I. Gut, R. Rebourcet, P. Laissue, et al. (2007)
Hypertension 49, 76-83
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Inositol Phosphoglycan P-Type in Preeclampsia: A Novel Marker?.
P. J. Williams, K. Gumaa, M. Scioscia, C. W. Redman, and T. W. Rademacher (2007)
Hypertension 49, 84-89
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Severe Feto-Placental Abnormalities Precede the Onset of Hypertension and Proteinuria in a Mouse Model of Preeclampsia.
A. Dokras, D. S. Hoffmann, J. S. Eastvold, M. F. Kienzle, L. M. Gruman, P. A. Kirby, R. M. Weiss, and R. L. Davisson (2006)
Biol Reprod 75, 899-907
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Soluble HLA-G1 inhibits angiogenesis through an apoptotic pathway and by direct binding to CD160 receptor expressed by endothelial cells.
P. Fons, S. Chabot, J. E. Cartwright, F. Lenfant, F. L'Faqihi, J. Giustiniani, J.-P. Herault, G. Gueguen, F. Bono, P. Savi, et al. (2006)
Blood 108, 2608-2615
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Differential Expression of FOXO1 and FOXO3a Confers Resistance to Oxidative Cell Death upon Endometrial Decidualization.
T. Kajihara, M. Jones, L. Fusi, M. Takano, F. Feroze-Zaidi, G. Pirianov, H. Mehmet, O. Ishihara, J. M. Higham, E. W.-F. Lam, et al. (2006)
Mol. Endocrinol. 20, 2444-2455
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Soluble endoglin and other circulating antiangiogenic factors in preeclampsia..
R. J. Levine, C. Lam, C. Qian, K. F. Yu, S. E. Maynard, B. P. Sachs, B. M. Sibai, F. H. Epstein, R. Romero, R. Thadhani, et al. (2006)
N. Engl. J. Med. 355, 992-1005
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Calcitonin gene-related peptide stimulates human villous trophoblast cell differentiation in vitro.
K.E. Green, C. Thota, G.D.V. Hankins, C. Yallampalli, and Y.-L. Dong (2006)
Mol. Hum. Reprod. 12, 443-450
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Decreased expression of the angiogenic regulators CYR61 (CCN1) and NOV (CCN3) in human placenta is associatedwith pre-eclampsia.
A. Gellhaus, M. Schmidt, C. Dunk, S. J. Lye, R. Kimmig, and E. Winterhager (2006)
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Hypoxia Inhibits Differentiation of Lineage-Specific Rcho-1 Trophoblast Giant Cells.
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Genetic polymorphisms of vascular endothelial growth factor in severe pre-eclampsia.
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Biol Reprod 74, 538-544
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Soluble Vascular Endothelial Growth Factor Receptor-1 (sFLT-1) Mediates Downregulation of FLT-1 and Prevents Activated Neutrophils From Women With Preeclampsia From Additional Migration by VEGF.
O. Krysiak, A. Bretschneider, E. Zhong, J. Webb, H. Hopp, S. Verlohren, N. Fuhr, M. Lanowska, A. Nonnenmacher, R. Vetter, et al. (2005)
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A. P. Williams, A. R. Bateman, and S. I. Khakoo (2005)
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