ArticleBlood2022
Erythroid overproduction of erythroferrone causes iron overload and developmental abnormalities in mice.
Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07612345 (Safety and Tolerability of Supratherapeutic Vitamin C Supplementation in Class A Glucose-6-Phosphate Dehydrogenase), which is not on this map. Cited by 23 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Safety and Tolerability of Supratherapeutic Vitamin C Supplementation in Class A Glucose-6-Phosphate Dehydrogenase (G6PD A) Deficiency and Pyruvate Kinase Deficiency (PKD)
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Myonectin and metabolic health: a systematic review.Frontiers in endocrinology · 2025Pooled it
- Metabolomic Investigation of Myelodysplastic Syndromes, Multiple Myeloma, and Homozygous β-Thalassemia.Cells · 2025Review
- Article
- Transgenic augmentation of erythroferrone in mice ameliorates anemia in adenine-induced chronic kidney disease.JCI insight · 2025Article
- Hereditary disorders of ineffective erythropoiesis.Blood cells, molecules & diseases · 2025Review
- Low-risk MDS-A spotlight on precision medicine forHemaSphere · 2025Review
- Outline of Iron Metabolism, with Emphasis on Erythroid Cells.Mediterranean journal of hematology and infectious diseases · 2025Review
- Article
- Activation of Intestinal HIF2α Ameliorates Iron-Refractory Anemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Mechanisms controlling cellular and systemic iron homeostasis.Nature reviews. Molecular cell biology · 2024Review
- Understanding iron homeostasis in MDS: the role of erythroferrone.Frontiers in oncology · 2024Review
- Ferroptosis as an emerging target in sickle cell disease.Current research in toxicology · 2024Article
- Article
- Erythroferrone exacerbates iron overload and ineffective extramedullary erythropoiesis in a mouse model of β-thalassemia.Blood advances · 2023Article
- Article
- Fighting age-related orthopedic diseases: focusing on ferroptosis.Bone research · 2023Review
- Managing the Dual Nature of Iron to Preserve Health.International journal of molecular sciences · 2023Review
- Iron as a therapeutic target in chronic liver disease.World journal of gastroenterology · 2023Review
- Functional role of endothelial transferrin receptor 1 in iron sensing and homeostasis.American journal of hematology · 2022Article
- Erythroferrone contributes to iron mobilization for embryo erythropoiesis in iron-deficient mouse pregnancies.American journal of hematology · 2022Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
The hormone erythroferrone (ERFE) is produced by erythroid cells in response to hemorrhage, hypoxia, or other erythropoietic stimuli, and it suppresses the hepatic production of the iron-regulatory hormone hepcidin, thereby mobilizing iron for erythropoiesis. Suppression of hepcidin by ERFE is believed to be mediated by interference with paracrine bone morphogenetic protein (BMP) signaling that regulates hepcidin transcription in hepatocytes. In anemias with ineffective erythropoiesis, ERFE is pathologically overproduced, but its contribution to the clinical manifestations of these anemias is not well understood. We generated 3 lines of transgenic mice with graded erythroid overexpression of ERFE and found that they developed dose-dependent iron overload, impaired hepatic BMP signaling, and relative hepcidin deficiency. These findings add to the evidence that ERFE is a mediator of iron overload in conditions in which ERFE is overproduced, including anemias with ineffective erythropoiesis. At the highest levels of ERFE overexpression, the mice manifested decreased perinatal survival, impaired growth, small hypofunctional kidneys, decreased gonadal fat depots, and neurobehavioral abnormalities, all consistent with impaired organ-specific BMP signaling during development. Neutralizing excessive ERFE in congenital anemias with ineffective erythropoiesis may not only prevent iron overload but may have additional benefits for growth and development.
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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.