Endothelial cell dysfunction

Sandra T. Davidge, Christianne J.M. De Groot, Robert N. Taylor

Research output: Chapter in Book/Report/Conference proceedingChapterAcademicpeer-review

5 Citations (Scopus)


The hypothesis that preeclampsia phenotypes result from endothelial cell dysfunction has been followed by decades of evidence demonstrating vascular dysfunction and augmented vascular reactivity in preeclampsia. Multiple studies have detected biomarkers of endothelial activation prior to overt disease. The concept that endothelial cell dysfunction plays a pathogenetic role in preeclampsia is widely accepted, and investigators are now seeking and identifying circulating mediators of vascular activation. In this chapter, vascular effects of placental microvesicles, leukocytes, cytokines, fatty acids, "antiangiogenic" factors and autoantibodies are reviewed. Also highlighted are theories that oxygen free radicals and other mediators of oxidative stress converge as pathological precursors to endothelial cell dysfunction. Characterization, and ultimate neutralization, of such factors should lead to novel therapeutic strategies to prevent or reduce the severity of preeclampsia.

Original languageEnglish
Title of host publicationChesley's Hypertensive Disorders in Pregnancy, Fourth Edition
PublisherElsevier Science
Number of pages27
ISBN (Electronic)9780124078666
Publication statusPublished - 1 Jan 2014


  • Antiangiogenic factors
  • Cytokines
  • Eicosanoids
  • Endothelial cell activation
  • Lipid peroxidation
  • Placental microvesicles
  • Reactive oxygen species

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