ArticleNature communications2021
Maternal iron deficiency perturbs embryonic cardiovascular development in mice.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Maternal micronutrient deficiency and congenital heart disease risk: A systematic review of observational studies.Birth defects research · 2022Pooled it
- Risk of stillbirth among pregnant women with anaemia in India: secondary analysis of multiple cohorts from the ICMR-SPIC consortium.The Lancet regional health. Southeast Asia · 2026Article
- Evaluating the Performance of Traditional Pharmacoepidemiologic and Machine Learning Models to Predict Pregnancies at Risk of Major Congenital Malformations.Birth defects research · 2026Article
- Postnatal Iron Supplementation Fails to Fully Rescue Brain Metal and Transcriptional Defects Caused by Nutrition-Based Gestational Iron Deficiency.The Journal of nutrition · 2026Article
- The Potential Physiologic Mechanisms by Which Early-Life Nutrition May Influence Type 2 Diabetes Pathophysiology in Humans.Annual review of nutrition · 2026Review
- Maternal-Fetal Crosstalk in Cardiovascular Programming: Linking the Intrauterine Environment to Lifelong Disease Risk.Journal of cardiovascular development and disease · 2026Review
- Article
- Congenital heart disease and folate pathway gene polymorphisms: findings from a North Indian cohort.BMC cardiovascular disorders · 2026Article
- Maternal obesity during pregnancy disrupts iron homeostasis and promotes fetal hypoxia in the mouse.The Journal of physiology · 2026Article
- Maternal nutritional imbalance during pregnancy and the development of fetal-origin cardiovascular diseases.Frontiers in nutrition · 2026Review
- Iron-sensitive RNA regulation by poly C-binding proteins.Nucleic acids research · 2025Article
- Relationship between maternal iron status and the risk of congenital heart defects: A case-control study.The Journal of international medical research · 2025Article
- Maternal Anaemia and Congenital Heart Disease in Offspring: A Case-Control Study Using Linked Electronic Health Records in the United Kingdom.BJOG : an international journal of obstetrics and gynaecology · 2025Article
- Feto-placental blood vessel development.Development (Cambridge, England) · 2025Review
- The Critical Role of Iron in Pregnancy, Puerperium, and Fetal Development.Journal of clinical medicine · 2025Review
- Why cells need iron: a compendium of iron utilisation.Trends in endocrinology and metabolism: TEM · 2024Review
- Iron Deficiency Anaemia in Pregnancy: A Narrative Review from a Clinical Perspective.Diagnostics (Basel, Switzerland) · 2024Review
- Dysregulation of miRNA-mRNA expression in fetal growth restriction in a caloric restricted mouse model.Scientific reports · 2024Article
- Molecular Pathways and Animal Models of Tetralogy of Fallot and Double Outlet Right Ventricle.Advances in experimental medicine and biology · 2024Review
- Molecular Pathways and Animal Models of Truncus Arteriosus.Advances in experimental medicine and biology · 2024Review
Corrections and comments
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Authors and funding
22 authors at 7 institutions in 3 countries.
Funding
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.
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Registered trials
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.