ArticleBlood2010
Dysfunction of the heme recycling system in heme oxygenase 1-deficient mice: effects on macrophage viability and tissue iron distribution.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers.
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
176 citing papers in PubMed, 266 citations in OpenAlex.
- Impact of altered heme oxygenase-1 in caring for preterm neonates: navigating the unknown.Pediatric research · 2026Review
- Impact of altered heme oxygenase-1 in caring for preterm neonates: navigating the unknown.Pediatric research · 2026Review
- Placental Iron Homeostasis: Navigating the Delicate Balance Between Transport and Ferroptosis.International journal of molecular sciences · 2026Review
- Canonical Notch2 signaling regulates development and maintenance of iron-recycling macrophages and iron homeostasis.Nature communications · 2026Article
- Spatial transcriptomic analyses highlight distinct erythroid niches in mice and humans.Nature genetics · 2026Article
- CD163Biomarker research · 2026Article
- Recent advances in the construction of humanized animal models and applications in translational medicine.Animal models and experimental medicine · 2026Review
- Iron Biology in Acute Kidney Injury: Catalytic Iron, Hepcidin-Ferroportin Axis, and NGAL-A Narrative Review.International journal of molecular sciences · 2026Review
- STING synergizes with TOX suppressing HO-1 expression to trigger ferroptosis in tumor-infiltrating CD8+ T cell and immunotherapy resistance.Nature communications · 2026Article
- XPR1 regulates fetal liver macrophage development, identity, and pyrenocyte clearance.The Journal of experimental medicine · 2026Article
- CD71Scandinavian journal of immunology · 2026Article
- Article
- Emerging Role of Splenic Macrophage in Malaria Pathogenesis and Immunity.Immunity, inflammation and disease · 2025Review
- Molecular and Immunometabolic Landscape of Erythrophagocytosis-induced Ferroptosis.Cardiovascular & hematological disorders drug targets · 2025Review
- Pilot study: In vitro reduction of hemoglobin from canine blood with hemoperfusion using the Cytosorb® adsorber.PloS one · 2025Article
- Ferroptosis in osteoarthritis: metabolic reprogramming, immunometabolic crosstalk, and targeted intervention strategies.Frontiers in immunology · 2025Review
- Peripheral human red blood cell development in human immune system mouse model with heme oxygenase-1 deficiency.Blood advances · 2024Article
- Examining Hemin and its Derivatives: Induction of Heme-Oxygenase-1 Activity and Oxidative Stress in Breast Cancer Cells through Collaborative Experimental Analysis and Molecular Dynamics Simulations.Journal of medicinal chemistry · 2024Article
- Iron regulates the quiescence of naive CD4 T cells by controlling mitochondria and cellular metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
116 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
To better understand the tissue iron overload and anemia previously reported in a human patient and mice that lack heme oxygenase-1 (HO-1), we studied iron distribution and pathology in HO-1(Hmox1)(-/-) mice. We found that resident splenic and liver macrophages were mostly absent in HO-1(-/-) mice. Erythrophagocytosis caused the death of HO-1(-/-) macrophages in in vitro experiments, supporting the hypothesis that HO-1(-/-) macrophages died of exposure to heme released on erythrophagocytosis. Rupture of HO-1(-/-) macrophages in vivo and release of nonmetabolized heme probably caused tissue inflammation. In the spleen, initial splenic enlargement progressed to red pulp fibrosis, atrophy, and functional hyposplenism in older mice, recapitulating the asplenia of an HO-1-deficient patient. We postulate that the failure of tissue macrophages to remove senescent erythrocytes led to intravascular hemolysis and increased expression of the heme and hemoglobin scavenger proteins, hemopexin and haptoglobin. Lack of macrophages expressing the haptoglobin receptor, CD163, diminished the ability of haptoglobin to neutralize circulating hemoglobin, and iron overload occurred in kidney proximal tubules, which were able to catabolize heme with HO-2. Thus, in HO-1(-/-) mammals, the reduced function and viability of erythrophagocytosing macrophages are the main causes of tissue damage and iron redistribution.
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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.