Research ArticleReproductive Biology

Nrf2 inactivation enhances placental angiogenesis in a preeclampsia mouse model and improves maternal and fetal outcomes

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Science Signaling  16 May 2017:
Vol. 10, Issue 479, eaam5711
DOI: 10.1126/scisignal.aam5711

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  • Antioxidant supplementation in pregnant women: Good or Bad?

    Preeclampsia is among the most feared pregnancy complications (affects 5 to 10% of pregnancies worldwide) for which there is still no effective treatment. Clinical manifestations such as hypertension and proteinuria resolve only after delivery of the placenta, though patients experience an increased risk of cardiovascular disease later in life (1). Since the degree of oxidative stress correlates with the severity of preeclampsia, reactive oxygen species (ROS) emerged as an attractive target in clinical trials ─ with poor outcomes (2, 3). Antioxidant supplements such as vitamin C and vitamin E did not reduce the risk and have even increased unexplained stillbirths (antepartum deaths from 24 weeks' gestation) (3).

    To address this discrepancy, Nezu et al. impaired the antioxidative stress response by deleting the Nrf2 gene in a mouse model for preeclampsia known as PAH (pregnancy-associated hypertension). While ROS production increased, surprisingly, the deletion made mice live longer and improved fetomaternal circulation. Nrf2-deficient PAH mice showed activation of a wide variety of placental genes that act in concert to facilitate the formation of new blood vessels through recruitment of immune cells and endothelial progenitors. These findings suggest the need to refine antioxidant treatment strategies; meanwhile, attention is drawn to a clinical trial that aims to lower...

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    Competing Interests: None declared.

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