Commentary 10.1172/JCI134272

The selfishly selfless placenta

Nermi L. Parrow1 and Robert E. Fleming1,2

1Department of Pediatrics and the

2Edward A. Doisy Department of Biochemistry and Molecular Biology, St. Louis University School of Medicine, St. Louis, Missouri, USA.

Address correspondence to: Robert Fleming, St. Louis University School of Medicine, Department of Pediatrics, 1465 S. Grand Avenue, St. Louis, Missouri 63104, USA. Phone: 314.977.9315; Email: robert.fleming@health.slu.edu.

Find articles by Parrow, N. in: JCI | PubMed | Google Scholar

1Department of Pediatrics and the

2Edward A. Doisy Department of Biochemistry and Molecular Biology, St. Louis University School of Medicine, St. Louis, Missouri, USA.

Address correspondence to: Robert Fleming, St. Louis University School of Medicine, Department of Pediatrics, 1465 S. Grand Avenue, St. Louis, Missouri 63104, USA. Phone: 314.977.9315; Email: robert.fleming@health.slu.edu.

Find articles by Fleming, R. in: JCI | PubMed | Google Scholar |

First published December 17, 2019 - More info

Published in Volume 130, Issue 2 on February 3, 2020
J Clin Invest. 2020;130(2):590–592. https://doi.org/10.1172/JCI134272.
© 2020 American Society for Clinical Investigation
First published December 17, 2019 - Version history

Although iron deficiency continues to pose a problem for pregnant women and fetal development, an incomplete understanding of placental adaptation to limited iron availability has hindered efforts to identify optimal supplementation strategies. In this issue of the JCI, Sangkhae et al. used mouse models and human placentas to explore maternal, placental, and fetal responses to alterations in iron status during pregnancy. The authors identified molecular mechanisms that limit placental ability to upregulate iron transport in the setting of severe iron deficiency and explored a potential marker of placental maladaptation.

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