Maternal iron deficiency perturbs embryonic cardiovascular development in mice
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Abstract: Congenital heart disease (CHD) is the most common class of human birth defects, with a prevalence of 0.9% of births. However, two-thirds of cases have an unknown cause, and many of these are thought to be caused by in utero exposure to environmental teratogens. Here we identify a potential teratogen causing CHD in mice: maternal iron deficiency (ID). We show that maternal ID in mice causes severe cardiovascular defects in the offspring. These defects likely arise from increased retinoic acid signalling in ID embryos. The defects can be prevented by iron administration in early pregnancy. It has also been proposed that teratogen exposure may potentiate the effects of genetic predisposition to CHD through gene–environment interaction. Here we show that maternal ID increases the severity of heart and craniofacial defects in a mouse model of Down syndrome. It will be important to understand if the effects of maternal ID seen here in mice may have clinical implications for women.
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Funder: Novo Nordisk; doi: https://doi.org/10.13039/501100004191
Funder: National Heart Foundation of Australia (Heart Foundation); doi: https://doi.org/10.13039/501100001030
Funder: NSW Health; doi: https://doi.org/10.13039/501100009287
Funder: Oxford University | John Fell Fund, University of Oxford (John Fell OUP Research Fund); doi: https://doi.org/10.13039/501100004789
Funder: The Federated Foundation
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Wellcome Trust (Wellcome) (098328, 098328)
RCUK | Medical Research Council (MRC) (MR/S01019X/1)