ArticleOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2011
Bone status in a mouse model of genetic hemochromatosis.
Article in Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 75 citations in OpenAlex.
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- The Interplay Between Bone Biology and Iron Metabolism: Molecular Mechanisms and Clinical Implications.Biomedicines · 2026Review
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- Increased Risk of Fracture Among Patients With Iron Overload: A Population-based Matched Cohort Study.The Journal of clinical endocrinology and metabolism · 2025Article
- Bone phenotype in male and female mice after knockdown of transferrin receptor 1 in osterix-expressing cells.JBMR plus · 2025Article
- Depletion of macrophages and osteoclast precursors mitigates iron overload-mediated bone loss.IUBMB life · 2025Article
- Lysosome-Iron-Mitochondria Axis in Osteoclasts: Iron as a Central Player.Research (Washington, D.C.) · 2025Review
- Ferroptosis and bone health: bridging the gap between mechanisms and therapy.Frontiers in immunology · 2025Review
- Bone phenotyping of murine hemochromatosis models with deficiencies of Hjv, Alk2, or Alk3: The influence of sex and the bone compartment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Emerging role of liver-bone axis in osteoporosis.Journal of orthopaedic translation · 2024Review
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- GPX4-mediated bone ferroptosis under mechanical stress decreased bone formation via the YAP-TEAD signalling pathway.Journal of cellular and molecular medicine · 2024Article
- Transferrin receptor 2 deficiency promotes macrophage polarization and inflammatory arthritis.Redox biology · 2023Article
- Fighting age-related orthopedic diseases: focusing on ferroptosis.Bone research · 2023Review
- Iron, Zinc, Copper, Cadmium, Mercury, and Bone Tissue.International journal of environmental research and public health · 2023Review
- Article
- Identification of Common Pathogenic Pathways Involved in Hemochromatosis Arthritis and Calcium Pyrophosphate Deposition Disease: a Review.Current rheumatology reports · 2022Review
- Metabolomics Coupled with Pathway Analysis Provides Insights into Sarco-Osteoporosis Metabolic Alterations and Estrogen Therapeutic Effects in Mice.Biomolecules · 2021Article
- Iron accumulation deteriorated bone loss in estrogen-deficient rats.Journal of orthopaedic surgery and research · 2021Article
- Despite Genetic Iron Overload,JBMR plus · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledGenetic hemochromatosis is a cause of osteoporosis; mechanisms leading to iron-related bone loss are not fully characterized. We assessed the bone phenotype of HFE (-/-) male mice, a mouse model of hemochromatosis. They had a phenotype of osteoporosis with low bone mass and alteration of the bone microarchitecture.
introductionGenetic hemochromatosis is a cause of osteoporosis. However, the mechanisms leading to iron-related bone loss are not fully characterized. Recent human data have not supported the hypothesis of hypogonadism involvement. The direct role of iron on bone metabolism has been suggested.
methodsOur aim was to assess the bone phenotype of HFE (-/-) male mice, a mouse model of human hemochromatosis, by using microcomputed tomography and histomorphometry. HFE (-/-) animals were sacrificed at 6 and 12 months and compared to controls.
resultsThere was a significant increase in hepatic iron concentration and bone iron content in HFE (-/-) mice. No detectable Perls' staining was found in the controls' trabeculae. Trabecular bone volume (BV/TV) was significantly lower in HFE (-/-) mice at 6 and 12 months compared to the corresponding wild-type mice: 9.88 ± 0.82% vs 12.82 ± 0.61% (p = 0.009) and 7.18 ± 0.68% vs 10.4 ± 0.86% (p = 0.015), respectively. In addition, there was an impairment of the bone microarchitecture in HFE (-/-) mice. Finally, we found a significant increase in the osteoclast number in HFE (-/-) mice: 382.5 ± 36.75 vs 273.4 ± 20.95 ¢/mm(2) (p = 0.004) at 6 months and 363.6 ± 22.35 vs 230.8 ± 18.7 ¢/mm(2) (p = 0.001) at 12 months in HFE (-/-) mice vs controls.
conclusionOur data show that HFE (-/-) male mice develop a phenotype of osteoporosis with low bone mass and alteration of the microarchitecture. They suggest that there is a relationship between bone iron overload and the increase of the osteoclast number in these mice. These findings are in accordance with clinical observations in humans exhibiting genetic hemochromatosis and support a role of excess iron in relation to genetic hemochromatosis in the development of osteoporosis in humans.
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