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Int. J. Mol. Sci. 2018, 19(5), 1496; https://doi.org/10.3390/ijms19051496

Oxidative Stress in Preeclampsia and Placental Diseases

1,2,3,4,†
,
1,2,3,4,†
,
1,2,3,4,* and 1,2,3,4
1
Institut National de la Santé Et de la Recherche Médicale, U1016, Institut Cochin, 75014 Paris, France
2
Centre National de la Recherche Scientifique, UMR8104, 75014 Paris, France
3
Département Développement, Génétique, Neurobiologie, Reproduction et Vieillissement, Université Paris Descartes, Sorbonne Paris Cité, 75014 Paris, France
4
Département Hospitalo-Universitaire Risques et Grossesse, PRES Sorbonne, 75014 Paris, France
These two authors contribute equally to this paper.
*
Author to whom correspondence should be addressed.
Received: 29 March 2018 / Revised: 9 May 2018 / Accepted: 11 May 2018 / Published: 17 May 2018
(This article belongs to the Special Issue Free Radicals and Oxidants in Pathogenesis)
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Abstract

Preeclampsia is a persistent hypertensive gestational disease characterized by high blood pressure and proteinuria, which presents from the second trimester of pregnancy. At the cellular level, preeclampsia has largely been associated with the release of free radicals by the placenta. Placenta-borne oxidative and nitrosative stresses are even sometimes considered as the major molecular determinants of the maternal disease. In this review, we present the recent literature evaluating free radical production in both normal and pathological placentas (including preeclampsia and other major pregnancy diseases), in humans and animal models. We then assess the putative effects of these free radicals on the placenta and maternal endothelium. This analysis was conducted with regard to recent papers and possible therapeutic avenues. View Full-Text
Keywords: preeclampsia; pregnancy; oxidative stress; placenta; vascular endothelium preeclampsia; pregnancy; oxidative stress; placenta; vascular endothelium
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Aouache, R.; Biquard, L.; Vaiman, D.; Miralles, F. Oxidative Stress in Preeclampsia and Placental Diseases. Int. J. Mol. Sci. 2018, 19, 1496.

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