Placental iron utilisation in fetal growth restriction: alterations in mitochondrial haem synthesis and iron-sulphur cluster assembly pathways.

Veronica B Botha, Heather C Murray, Siddharth Acharya, Kirsty G Pringle, Roger Smith, Joshua J Fisher

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Article in The Journal of physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Veronica B BothaSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, New South Wales, Australia.

Heather C MurraySchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, New South Wales, Australia.

Siddharth AcharyaSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, New South Wales, Australia.

Kirsty G PringleSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, New South Wales, Australia.

Roger SmithSchool of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.

Joshua J FisherSchool of Medicine and Public Health, University of Newcastle, Callaghan, New South Wales, Australia.

Funding

National Health and Medical Research Council GNT2026065

6 · The paper itself

Abstract

Fetal growth restriction (FGR) affects ∼10% of pregnancies worldwide and is often associated with placental insufficiency. Iron is essential for maternal haematopoietic adaptations and placental processes such as mitochondrial iron-sulphur (Fe-S) cluster assembly, haem synthesis and erythropoiesis. This study aimed to characterise iron transport and downstream utilisation in FGR. Placental tissues from term uncomplicated (n = 19) and FGR (n = 18) pregnancies were analysed. Maternal iron status was retrospectively assessed from clinical records. Placental mRNA and protein expression of iron-dependent pathways were analysed via RT-qPCR, LC-MS and western blotting. Placental iron content was assessed histologically, and haem levels were measured by an activity assay. FGR pregnancies showed significantly elevated maternal serum ferritin and lower red cell distribution width, although these remained within normal clinical values. Placental iron uptake transporters TFRC and DMT1 were significantly upregulated, while the iron exporter to the fetus, ferroportin, was reduced, indicating increased iron retention in the FGR placenta. Despite altered transporter expression, Fe

Indexed as

Fetal Growth RetardationIronIron-Sulfur ProteinsMitochondriaPlacentaAdultFemaleHumansPregnancyIronIron-Sulfur Proteinserythrocyte structurefetal growth restrictionhaem synthesisiron–sulphur clustersiron transportmitochondriaplacenta

Identifiers

PMID41697720

DOI10.1113/JP289451

PMCPMC12953020

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.