ArticleMolecular medicine (Cambridge, Mass.)2025
Perinatal hypoxia-mediated neurodevelopment abnormalities in congenital heart disease mouse model.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundCyanotic congenital heart disease (CHD) in children has been associated with neurodevelopmental abnormalities, although the underlying mechanisms remain largely unknown. Multiple factors are likely involved in this process. This research aims to explore the potential effects of hypoxia and vascular system-derived factors in neurodevelopmental outcomes in offspring.
methodsMouse aorta endothelial cells (MEC) and amygdala neurons were isolated to investigate the effects of hypoxia on pro-inflammatory cytokine release, gene expression, redox balance, mitochondrial function, and epigenetic modifications. A CHD mouse model was established to evaluate the impact of perinatal hypoxia on fetal brain development. Estrogen receptor β (ERβ) expression in endothelial cells was modulated using Tie2-driven lentivirus both in vitro and in vivo study to assess the vascular system's contribution to hypoxia-mediated neurodevelopmental abnormalities.
resultsHypoxia exposure, along with factors released from MEC, led to altered gene expression, oxidative stress, mitochondrial dysfunction, and epigenetic modifications in amygdala neurons. In the CHD mouse model, perinatal hypoxia resulted in compromised vascular function, altered gene expression, disrupted redox balance in brain tissues, and impaired behavioral outcomes in offspring. Prenatal expression of ERβ in endothelial cells partially ameliorated these neurodevelopmental abnormalities, while prenatal knockdown of ERβ mimicked the effects of perinatal hypoxia.
conclusionsHypoxia, combined with endothelial cell-derived factors, induces epigenetic changes in neurons. In the CHD mouse model, perinatal hypoxia causes vascular dysfunction, altered gene expression, and redox imbalance in brain tissues, leading to behavioral impairments in offspring. Prenatal expression of ERβ in endothelial cells mitigates these effects, suggesting that modulating gene expression in the vascular system during pregnancy could play a protective role against hypoxia-induced neurodevelopmental abnormalities in CHD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.