ArticleThe American journal of pathology2000
Iron overload and heart fibrosis in mice deficient for both beta2-microglobulin and Rag1.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- IRP1 deficiency promotes fibroblast activation through iron dysregulation: protective modulation by HMolecular and cellular biochemistry · 2026Article
- Combined use of magnetic microbeads for endothelial cell isolation and enhanced cell engraftment in myocardial repair.Theranostics · 2023Article
- Article
- Review
- Characterization of Associated Nonclassical Phenotypes in Patients with Deletion in the WAGR Region Identified by Chromosomal Microarray: New Insights and Literature Review.Molecular syndromology · 2022Article
- Iron accumulation with age alters metabolic pattern and circadian clock gene expression through the reduction of AMP-modulated histone methylation.The Journal of biological chemistry · 2022Article
- Article
- HFE Related Hemochromatosis: Uncovering the Inextricable Link between Iron Homeostasis and the Immunological System.Pharmaceuticals (Basel, Switzerland) · 2019Article
- TIMP3 deficiency exacerbates iron overload-mediated cardiomyopathy and liver disease.American journal of physiology. Heart and circulatory physiology · 2018Article
- The hemochromatosis protein HFE 20 years later: An emerging role in antigen presentation and in the immune system.Immunity, inflammation and disease · 2017Review
- Post-mortem study of the association between cardiac iron and fibrosis in transfusion dependent anaemia.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2017Article
- The role of MHC class Ib-restricted T cells during infection.Immunogenetics · 2016Review
- Continuing treatment with Salvia miltiorrhiza injection attenuates myocardial fibrosis in chronic iron-overloaded mice.PloS one · 2015Article
- Brain iron homeostasis: from molecular mechanisms to clinical significance and therapeutic opportunities.Antioxidants & redox signaling · 2014Review
- Physiological implications of NTBI uptake by T lymphocytes.Frontiers in pharmacology · 2014Article
- Non-transferrin-bound iron (NTBI) uptake by T lymphocytes: evidence for the selective acquisition of oligomeric ferric citrate species.PloS one · 2013Article
- Hepcidin messenger RNA expression in human lymphocytes.Immunology · 2010Article
- Ceruloplasmin protects injured spinal cord from iron-mediated oxidative damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Iron overload and immunity.World journal of gastroenterology · 2007Review
- Overexpression of iron regulatory protein 1 suppresses growth of tumor xenografts.Carcinogenesis · 2007Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic causes of hereditary hemochromatosis (HH) include mutations in the HFE gene, a ss2-microglobulin (ss2m)-associated major histocompatibility complex class I-like protein. Accordingly, mutant ss2m(-/-) mice have increased intestinal iron absorption and develop parenchymal iron overload in the liver. In humans, other genetic and environmental factors have been suggested to influence the pathology and severity of HH. Previously, an association has been reported between low numbers of lymphocytes and the severity of clinical expression of the iron overload in HH. In the present study, the effect of a total absence of lymphocytes on iron overload was investigated by crossing ss2m(-/-) mice (which develop iron overload resembling human disease) with mice deficient in recombinase activator gene 1 (Rag1), which is required for normal B and T lymphocyte development. Iron overload was more severe in ss2mRag1 double-deficient mice than in each of the single deficient mice, with iron accumulation in parenchymal cells of the liver, in acinar cells of the pancreas, and in heart myocytes. With increasing age ss2mRag1(-/-) mice develop extensive heart fibrosis, which could be prevented by reconstitution with normal hematopoietic cells. Thus, the development of iron-mediated cellular damage is substantially enhanced when a Rag1 mutation, which causes a lack of mature lymphocytes, is introduced into ss2m(-/-) mice. Mice deficient in ss2m and Rag1 thus offer a new experimental model of iron-related cardiomyopathy.
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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.