2005
DOI: 10.1210/jc.2005-0078
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Molecular Evidence of Placental Hypoxia in Preeclampsia

Abstract: Our results provide molecular evidence that aberrant global placental gene expression changes in preeclampsia may be due to reduced oxygenation and that these events can successfully be mimicked by in vivo and in vitro models of placental hypoxia.

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Cited by 336 publications
(280 citation statements)
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“…Oxygen is one of the key elements in cell metabolism, and its concentration in tissues plays an important role in regulating biochemical reactions , Soleymanlou et al, 2005.…”
Section: Introductionmentioning
confidence: 99%
“…Oxygen is one of the key elements in cell metabolism, and its concentration in tissues plays an important role in regulating biochemical reactions , Soleymanlou et al, 2005.…”
Section: Introductionmentioning
confidence: 99%
“…Poor placental perfusion appears to result in a cascade of pathological changes: decreased oxygen delivery (6)(7)(8)(9), oxidative stress, formation of reactive oxygen species, endothelial damage (10), increased vascular permeability (11), and inflammation. The role of oxidative stress in PE has been studied by many investigators.…”
Section: Introductionmentioning
confidence: 99%
“…The main source of ROS initiating the pathophysiological events appears to be the placenta [8]. Abnormal vascular development of the blood vessels in the preeclamptic placenta leads to reduced placental perfusion and to induce hypoxia which is by itself a potent stimulus for ROS formation [9]. Also, after initiation of apoptotic pathways, syncytiotrophoblast microvesicles activate maternal neutrophils contributing to oxidative stress and pathophysiology of PE.…”
mentioning
confidence: 99%