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Angiotensin Receptors, Autoimmunity, and Preeclampsia¹

Yang Xia^2,*, Cissy Chenyi Zhou^*, Susan M. Ramin and Rodney E. Kellems^*

^* Department of Biochemistry and Molecular Biology and Department of Obstetrics Gynecology and Reproductive Sciences, University of Texas Medical School, Houston, TX 77030

Preeclampsia is a pregnancy-induced hypertensive disorder that causes substantial maternal and fetal morbidity and mortality. Despite being a leading cause of maternal death and a major contributor to maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of preeclampsia are poorly understood. Recent studies indicate that women with preeclampsia have autoantibodies that activate the angiotensin receptor, AT1, and that autoantibody-mediated receptor activation contributes to pathophysiology associated with preeclampsia. The research reviewed here raises the intriguing possibility that preeclampsia may be a pregnancy-induced autoimmune disease.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants HL076558 (to Y.X) and HD34130 (to R.E.K) and grants from the March of Dimes Foundation (6-FY06-323) and the Texas Higher Education Coordinating Board (to R.E.K.).

² Address correspondence and reprint requests to Dr. Yang Xia, Department of Biochemistry and Molecular Biology, University of Texas Health Science Center at Houston, Medical School, 6431 Fannin Street, Houston, TX 77030. E-mail address: yang.xia{at}uth.tmc.edu

³ Abbreviations used in this paper: AT1-AA, AT1 receptor agonistic antibody; Ang II, angiotensin II; GPCR, G protein-coupled receptor; PAI-1, plasminogen activator inhibitor-1; sFlt-1, soluble fms-like tyrosine kinase-1; RUPP, reduced uterine perfusion pressure.

This article has been cited by other articles:

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