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Maternal iron deficiency perturbs embryonic cardiovascular development in mice

Author

Listed:
  • 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
    Walter and Eliza Hall Institute of Medical Research)

  • Michael Troup

    (Molecular, Structural and Computational Biology Division)

  • Shelley E. Harris

    (University of Oxford
    University of Southampton)

  • Helena Rodriguez-Caro

    (University of Oxford)

  • Aimée Jacquemot

    (University of Oxford
    Ealing Hospital)

  • Jack J. Miller

    (University of Oxford
    University of Oxford
    John Radcliffe Hospital
    Aarhus University)

  • Eleanor M. Stuart

    (University of Oxford
    University of Cambridge)

  • Magda Wolna

    (University of Oxford)

  • Emily Hardman

    (The Francis Crick Institute
    University of Manchester)

  • Fabrice Prin

    (The Francis Crick Institute
    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
    Imperial College London)

  • Timothy J. Mohun

    (The Francis Crick Institute)

  • Samira Lakhal-Littleton

    (University of Oxford)

  • Sarah De Val

    (University of Oxford
    University of Oxford)

  • Eleni Giannoulatou

    (Molecular, Structural and Computational Biology Division
    University of New South Wales)

  • Duncan B. Sparrow

    (University of Oxford)

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.

Suggested Citation

  • 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 & , 2021. "Maternal iron deficiency perturbs embryonic cardiovascular development in mice," Nature Communications, Nature, vol. 12(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-23660-5
    DOI: 10.1038/s41467-021-23660-5
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