Maternal iron deficiency perturbs embryonic cardiovascular development in mice

Jacinta I. Kalisch-Smith, Nikita Ved, Dorota Szumska, Jacob Munro, Michael Troup, Shelley E. Harris, Helena Rodriguez-Caro, Aimée Jacquemot, Jack J. Miller, Eleanor M. Stuart, Magda Wolna, Emily Hardman, Fabrice Prin, Eva Lana-Elola, Rifdat Aoidi, Elizabeth M. C. Fisher, Victor L. J. Tybulewicz, Timothy J. Mohun, Samira Lakhal-Littleton, Sarah De Val, Eleni Giannoulatou and Duncan B. Sparrow ()
Additional contact information
Jacinta I. Kalisch-Smith: University of Oxford
Nikita Ved: University of Oxford
Dorota Szumska: University of Oxford
Jacob Munro: Molecular, Structural and Computational Biology Division
Michael Troup: Molecular, Structural and Computational Biology Division
Shelley E. Harris: University of Oxford
Helena Rodriguez-Caro: University of Oxford
Aimée Jacquemot: University of Oxford
Jack J. Miller: University of Oxford
Eleanor M. Stuart: University of Oxford
Magda Wolna: University of Oxford
Emily Hardman: The Francis Crick Institute
Fabrice Prin: The Francis Crick Institute
Eva Lana-Elola: The Francis Crick Institute
Rifdat Aoidi: The Francis Crick Institute
Elizabeth M. C. Fisher: University College London
Victor L. J. Tybulewicz: The Francis Crick Institute
Timothy J. Mohun: The Francis Crick Institute
Samira Lakhal-Littleton: University of Oxford
Sarah De Val: University of Oxford
Eleni Giannoulatou: Molecular, Structural and Computational Biology Division
Duncan B. Sparrow: University of Oxford

Nature Communications, 2021, vol. 12, issue 1, 1-17

Abstract: 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.

Date: 2021
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DOI: 10.1038/s41467-021-23660-5

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