ArticleCommunications biology2024
Atoh1 mediated disturbance of neuronal maturation by perinatal hypoxia induces cognitive deficits.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Prenatal Delivery of HIF-1α siRNA Using Transferrin-Modified Lipid Nanoparticles Alleviates Hypoxia-Induced Neurodevelopmental Abnormalities via PTEN/PI3K/AKT Signaling.International journal of nanomedicine · 2026Article
- Fto-mediated mJournal of biomedical science · 2025Article
- Association between neurodevelopmental disorders in congenital heart disease and changes in circulatory metabolites and gut microbiota composition.Frontiers in microbiology · 2025Article
- Unraveling the complexity of cognitive impairment following high-altitude exposure: from preclinical animal models to human organoids.Frontiers in neuroscience · 2025Review
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Authors and funding
11 authors.
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Abstract
Neurodevelopmental disorders are currently one of the major complications faced by patients with congenital heart disease (CHD). Chronic hypoxia in the prenatal and postnatal preoperative brain may be associated with neurological damage and impaired long-term cognitive function, but the exact mechanisms are unknown. In this study, we find that delayed neuronal migration and impaired synaptic development are attributed to altered Atoh1 under chronic hypoxia. This is due to the fact that excessive Atoh1 facilitates expression of Kif21b, which causes excess in free-state α-tubulin, leading to disrupted microtubule dynamic stability. Furthermore, the delay in neonatal brain maturation induces cognitive disabilities in adult mice. Then, by down-regulating Atoh1 we alleviate the impairment of cell migration and synaptic development, improving the cognitive behavior of mice to some extent. Taken together, our work unveil that Atoh1 may be one of the targets to ameliorate hypoxia-induced neurodevelopmental disabilities and cognitive impairment in CHD.
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