Expert Reviews in Molecular Medicine: http://www.expertreviews.org/
DOI: 10.1017/S1462399406010465; 27 January 2006
Sowndramalingam Sankaralingam, Ivan A. Arenas, Manoj M. Lalu and Sandra T. Davidge (2006) Preeclampsia: current understanding of the molecular basis of vascular dysfunction.
Expert Rev. Mol. Med. Vol. 8, Issue 3, DOI: 10.1017/S1462399406010465

Preeclampsia: current understanding of the molecular basis of vascular dysfunction

Sowndramalingam Sankaralingam, Ivan A. Arenas, Manoj M. Lalu and Sandra T. Davidge

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Preeclampsia is a pregnancy-specific disorder characterised by hypertension and proteinuria occurring after the 20th week of gestation. Delivery of the placenta results in resolution of the condition, implicating the placenta as a central culprit in the pathogenesis of preeclampsia. In preeclampsia, an inadequate placental trophoblast invasion of the maternal uterine spiral arteries results in poor placental perfusion, leading to placental ischaemia. This could result in release of factors into the maternal circulation that cause widespread activation or dysfunction of the maternal endothelium. Factors in the maternal circulation might induce oxidative stress and/or elicit an inflammatory response in the maternal endothelium, resulting in the altered expression of several genes involved in the regulation of vascular tone. This review addresses the potential circulating factors and the molecular mechanisms involved in the alteration of vascular function that occurs in preeclampsia.

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Figure 1. Role of oxidative stress in the mediation of endothelial cell dysfunction in preeclampsia.
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Figure 2. L-arginine depletion generates superoxide by uncoupling of eNOS.
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