Maternal iron deficiency perturbs embryonic cardiovascular development in mice

Kalisch-Smith, Jacinta I. and Ved, Nikita and Szumska, Dorota and Munro, Jacob and Troup, Michael and Harris, Shelley E. and Rodriguez-Caro, Helena and Jacquemot, Aimée and Miller, Jack J. and Stuart, Eleanor M. and Wolna, Magda and Hardman, Emily and Prin, Fabrice and Lana-Elola, Eva and Aoidi, Rifdat and Fisher, Elizabeth M. C. and Tybulewicz, Victor L. J. and Mohun, Timothy J. and Lakhal-Littleton, Samira and De Val, Sarah and Giannoulatou, Eleni and Sparrow, Duncan B. (2021) Maternal iron deficiency perturbs embryonic cardiovascular development in mice. Nature Communications, 12 (1). ISSN 2041-1723

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Link to published document: http://doi.org/10.1038/s41467-021-23660-5

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.

Item Type: Article
Subjects: R Medicine > R Medicine (General)
Depositing User: Repository Administrator
Date Deposited: 31 Jul 2021 05:12
Last Modified: 01 Aug 2021 04:27
URI: http://eprints.victorchang.edu.au/id/eprint/1088

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