Gestational chronic intermittent hypoxia triggers maternal inflammation and disrupts placental stress responses

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Abstract

Late-gestation exposure to even mild, short-term, chronic intermittent hypoxia (CIH) is sufficient to initiate maternal inflammation and disrupt key placental stress response mechanisms, despite occurring after placental development is largely complete. These findings highlight a novel temporal maternal and placental vulnerability in late pregnancy and identify novel targets for understanding the pathophysiology of hypoxia-related pregnancy complications.

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