ArticleNature communications2024
Increased iron uptake by splenic hematopoietic stem cells promotes TET2-dependent erythroid regeneration.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed.
- Canonical Notch2 signaling regulates development and maintenance of iron-recycling macrophages and iron homeostasis.Nature communications · 2026Article
- Glycosylation orchestrates megakaryocytic fate of hematopoietic stem cells via Wnt-MUC13 signaling.Nature communications · 2026Article
- Intermittent oral administration of iron oxide nanoparticles modulates iron homeostasis, hematological, inflammatory, and organ-specific responses in iron-deficient rats.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Molecular and therapeutic frontiers in anemia therapy.The Journal of clinical investigation · 2026Review
- Article
- Signaling mechanisms and cis -regulatory control of Samd14 in erythroid regeneration.Current opinion in hematology · 2025Review
- Regeneration alters open chromatin andGenome research · 2025Article
- Haematometabolism rewiring in atherosclerotic cardiovascular disease.Nature reviews. Cardiology · 2025Review
- Itaconate promotes the differentiation of murine stress erythroid progenitors by increasing Nrf2 activity.Blood. Red cells & iron · 2025Article
- Guanine nucleotide biosynthesis blockade impairs MLL complex formation and sensitizes leukemias to menin inhibition.Nature communications · 2025Article
- MFSD7C protects hemolysis-induced lung impairments by inhibiting ferroptosis.Nature communications · 2024Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Hematopoietic stem cells (HSCs) are capable of regenerating the blood system, but the instructive cues that direct HSCs to regenerate particular lineages lost to the injury remain elusive. Here, we show that iron is increasingly taken up by HSCs during anemia and induces erythroid gene expression and regeneration in a Tet2-dependent manner. Lineage tracing of HSCs reveals that HSCs respond to hemolytic anemia by increasing erythroid output. The number of HSCs in the spleen, but not bone marrow, increases upon anemia and these HSCs exhibit enhanced proliferation, erythroid differentiation, iron uptake, and TET2 protein expression. Increased iron in HSCs promotes DNA demethylation and expression of erythroid genes. Suppressing iron uptake or TET2 expression impairs erythroid genes expression and erythroid differentiation of HSCs; iron supplementation, however, augments these processes. These results establish that the physiological level of iron taken up by HSCs has an instructive role in promoting erythroid-biased differentiation of HSCs.
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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.