ArticleJournal of orthopaedic surgery and research2024
Iron accumulation induced by hepcidin1 knockout accelerates the progression of aging osteoporosis.
Article in Journal of orthopaedic surgery and research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed.
- Biomarkers of Inflammaging and Cellular Senescence in Musculoskeletal (MSK) Diseases: The Knowns and the Unknowns.Biomedicines · 2026Article
- D-galactose-induced osteoporosis in rodents-Model development, skeletal characteristics, and optimal dosing regimens: A scoping review.Biomolecules & biomedicine · 2026Article
- Association of serum ferritin with bone turnover markers and bone mineral density in children and adolescents: Finding from NHANES 1999-2002.The Journal of international medical research · 2026Article
- Article
- Fat Fraction and Iron Concentration in Lumbar Vertebral Bone Marrow in the UK Biobank.Obesity science & practice · 2025Article
- LINC01133 promotes the osteogenic differentiation of bone marrow mesenchymal stem cells by upregulating CTNNB1 by acting as a sponge for miR-214-3p.Journal of orthopaedic surgery and research · 2024Article
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Abstract
objectiveIron accumulation is associated with osteoporosis. This study aims to explore the effect of chronic iron accumulation induced by hepcidin1 deficiency on aging osteoporosis.
methodsIron accumulation in hepcidin1 knockout aging mice was assessed by atomic absorption spectroscopy and Perl's staining. Bone microarchitecture was observed using Micro-CT. Hepcidin, ferritin, oxidative stress, and markers of bone turnover in serum were detected by enzyme-linked immunosorbent assay. Bone formation and resorption markers were measured by real-time quantitative PCR. Cell aging was induced by D-galactose treatment. CCK-8, flow cytometry, EdU assays, and Alizarin red staining were performed to reveal the role of hepcidin1 knockout in cell model. Iron Colorimetric Assay Kit and western blot were applied to detect iron and ferritin levels in cells, respectively.
resultsIn hepcidin1-knockout mice, the ferritin and iron contents in liver and tibia were significantly increased. Iron accumulation induced by hepcidin1 knockout caused a phenotype of low bone mass and deteriorated bone microarchitecture. Osteogenic marker was decreased and osteoclast marker was increased in mice, accompanied by increased oxidative stress level. The mRNA expression levels of osteoclast differentiation markers (RANKL, Mmp9, OPG, Trap, and CTSK) were up-regulated, while bone formation markers (OCN, ALP, Runx2, SP7, and Col-1) were down-regulated in model group, compared to wild type mice. In vitro, hepcidin1 knockdown inhibited proliferation and osteogenic differentiation, while promoted apoptosis, with increased levels of iron and ferritin.
conclusionIron accumulation induced by hepcidin1 deficiency aggravates the progression of aging osteoporosis via inhibiting osteogenesis and promoting osteoclast genesis.
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