Semin Reprod Med 1998; 16(1): 17-31
DOI: 10.1055/s-2007-1016249
Copyright © 1998 by Thieme Medical Publishers, Inc.

Circulating Factors as Markers and Mediators of Endothelial Cell Dysfunction in Preeclampsia

Robert N. Taylor* , Christianne J.M. de Groot*, , Yong K. Cho*, , Kee-Hak Lim*
  • *Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California, San Francisco, California;
  • †Department of Obstetrics and Gynecology, University Hospital, Leiden, The Netherlands; and
  • ‡Department of Obstetrics and Gynecology, Inje University, Seoul, Korea
Further Information

Publication History

Publication Date:
15 March 2008 (online)

Abstract

During the past decade a new hypothesis has been formulated that explains many of the disparate findings associated with the pregnancy syndrome preeclampsia. With an increased awareness of the physiological significance of vascular endothelial cell function, the seemingly unrelated signs of hypertension, proteinuria, edema, and hypercoagulability have converged to provide clinical evidence of a unifying pathophysiological mechanism: systemic, maternal endothelial cell dysfunction. Investigators have attempted to test this hypothesis through two approaches. The first approach involves the identification of in vivo markers of vascular endothelial cell injury in women with clinically evident preeclampsia. The second approach focuses on the ability of circulating factors derived from the serum or plasma of patients afflicted with preeclampsia to perturb endothelial cell function in vitro. In this review we summarize the increasingly compelling evidence that maternal vascular endothelial cells are a critical target for toxic humoral activities that precipitate the multifaceted preeclampsia syndrome.