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(Hypertension. 2007;50:35.)
© 2007 American Heart Association, Inc.
Editorial Commentaries |
From the Departments of Obstetrics & Gynecology and Medicine, Division of Biological Sciences (M.D.L.), University of Chicago, Ill; Perinatology Research Branch (R.R.), Division of Intramural Research, National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, Bethesda, Md; and the Center for Molecular Medicine and Genetics (R.R.), Wayne State University School of Medicine, Detroit, Mich.
Correspondence to Marshall D. Lindheimer, Departments of OB/GYN & Medicine, Division of Biological Sciences, University of Chicago, IL 60637. E-mail mlindhei@medicine.bsd.uchicago.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Hypertensive disorders are a major cause of maternal and fetal death, especially in developing nations, with the pregnancy-specific disease preeclampsia-eclampsia responsible for most of this mortality. Preeclampsia, recognized by ancient Greeks, was only sporadically investigated until late last century, current literature still labeling this disorder a "disease of theories." Thus, not surprisingly, we have started the new millennium unable to predict or prevent preeclampsia, and management strategies remain but supportive, with pregnancy termination still the only definitive "therapy." This may be about to change, as focused research, mainly in the past decade, has resulted in dramatic progress regarding pathogenesis of disease manifestations and risk assessment, while investigators have begun designing and testing definitive therapy.1 There are still a myriad of uncertainties and unanswered questions to address, but here we summarize the extent of 1 new and exciting chapter in preeclampsia research: the roles of angiogenic and antiangiogenic factors, to which an article in this issue by Rana and colleagues,2 contributes.
A landmark report published in 2003 set the stage for all that followed.3 Dr Karumanchis laboratory, previously involved in renal cancer research, changed its focus to the kidney in preeclampsia. Using microarray chip technology, they probed gene expression profiles in placentas of women with preeclampsia and those with uncomplicated pregnancies. Of course many differences were noted, but one that caught the investigators attention was upregulation of the mRNA for the antiangiogenic protein soluble fms-like tyrosine kinase 1 (abbreviated as sFlt-1 or sVEGFR-1) in placentas from women with preeclampsia. Aware that
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