ArticlePediatric research2022
Low maternal vitamin A intake increases the incidence of teratogen induced congenital diaphragmatic hernia in mice.
Article in Pediatric research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- The nitrofen/bisdiamine murine model of congenital diaphragmatic hernia has a pulmonary hypertension vascular phenotype consistent with human CDH.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Mesenchymal retinoic acid signaling is required for normal diaphragm development in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The etiology of congenital diaphragmatic hernia: the retinoid hypothesis 20 years later.Pediatric research · 2024Review
- Role of genetics and the environment in the etiology of congenital diaphragmatic hernia.World journal of pediatric surgery · 2024Review
- Review
- Characterization of the congenital diaphragmatic hernia model in C57BL/6J fetal mice: a step toward lineage tracing experiments.Pediatric surgery international · 2023Article
- Connecting clinical, environmental, and genetic factors point to an essential role for vitamin A signaling in the pathogenesis of congenital diaphragmatic hernia.American journal of physiology. Lung cellular and molecular physiology · 2023Review
- The role of genes and environment in the etiology of congenital diaphragmatic hernias.Current topics in developmental biology · 2023Review
- Signaling through retinoic acid receptors is essential for mammalian uterine receptivity and decidualization.JCI insight · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCongenital diaphragmatic hernia (CDH) is a severe birth defect associated with high perinatal mortality and long-term morbidity. The etiology of CDH is poorly understood although abnormal retinoid signaling has been proposed to contribute to abnormal diaphragm development. Existing epidemiological data suggest that inadequate dietary vitamin A intake is a risk factor for developing CDH.
methodsUsing a mouse model of teratogen-induced CDH, the objective of this study was to test the hypothesis that low maternal vitamin A intake contributes to abnormal diaphragm development. To test this hypothesis, we optimized a model of altered maternal dietary vitamin A intake and a teratogenic model of CDH in mice that recapitulates the hallmark features of posterolateral diaphragmatic hernia in humans.
resultsOur data uniquely show that low maternal dietary vitamin A intake and marginal vitamin A status increases the incidence of teratogen-induced CDH in mice.
conclusionLow dietary vitamin A intake and marginal vitamin A status lead to an increased incidence of teratogen-induced CDH in mice, highlighting the importance of adequate dietary vitamin A intake and CDH risk. IMPACT: This study describes and validates a mouse model of altered maternal and fetal vitamin A status. This study links existing epidemiological data with a mouse model of teratogen-induced congenital diaphragmatic hernia, highlighting the importance of low maternal vitamin A intake as a risk factor for the development of congenital diaphragmatic hernia. This study supports the Retinoid Hypothesis, which posits that the etiology of congenital diaphragmatic hernia is linked to abnormal retinoid signaling in the developing diaphragm.
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