Demonstrates uterine artery remodelling and altered reactivity in rodent hypoxic pregnancy, suggesting mitochondrial pathways as therapeutic targets.
Gestational hypoxia adversely affects uterine artery function, increasing complications. However, an effective therapy remains unidentified. Here, we show in rodent uterine arteries that hypoxic pregnancy promotes hypertrophic remodelling, increases constrictor reactivity via protein kinase C signalling, and triggers compensatory dilatation via nitric oxide-dependent mechanisms and stimulation of large conductance Ca
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Wang et al. (2024) studied this question.
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