ArticleAmerican journal of physiology. Cell physiology2025
Gestational chronic intermittent hypoxia triggers maternal inflammation and disrupts placental stress responses.
Article in American journal of physiology. Cell physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Prenatal methylmercury exposure disrupts developmental trajectories and induces sex-specific toxicity in pubertal rats.Research square · 2026Article
- Fetal sex shapes placental inflammatory responses to extracellular mitochondrial DNA.bioRxiv : the preprint server for biology · 2026Article
- Acute exposure to cell-free mitochondrial DNA induces pregnancy-specific aortic endothelial dysfunction and organ-selective inflammation in rats.bioRxiv : the preprint server for biology · 2026Article
- The Role of HIF-1α and Its Association with BDNF Levels in Post-Stroke Cognitive Decline Following Prenatal Immune Activation and Maternal Hypoxic Stress in Adult Rat Offspring: A Sex Comparison Study.Molecular neurobiology · 2026Article
- Extracellular vesicles in preeclampsia: drivers of vascular dysfunction and inflammation.American journal of physiology. Heart and circulatory physiology · 2025Review
- Preliminary Evidence Linking Maternal Sleep-Disordered Breathing During Pregnancy to Early Childhood Development: A 3-Year Pilot Cohort Study in Japan.Children (Basel, Switzerland) · 2025Article
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Abstract
Gestational hypoxia is associated with placental cellular responses, including oxidative stress and inflammation. Circulating cell-free mitochondrial DNA (ccf-mtDNA) is a marker of cell stress that can be transported within extracellular vehicles (EVs), eliciting proinflammatory responses. We hypothesized that systemic exposure to chronic intermittent hypoxia (CIH) during late pregnancy would increase maternal inflammation, alter circulating EV characteristics, and disrupt placental stress responses. Pregnant rats were exposed to CIH (
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