ArticleInflammation2015
Effects of mouse hepcidin 1 treatment on osteoclast differentiation and intracellular iron concentration.
Article in Inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 18 citations in OpenAlex.
- Iron and Bone Pathophysiology.Advances in experimental medicine and biology · 2025Review
- The Role of Mitochondrial Regulation in Macrophage Polarization: Implications for the Pathogenesis of Rheumatoid Arthritis.Journal of inflammation research · 2025Review
- Emerging role of liver-bone axis in osteoporosis.Journal of orthopaedic translation · 2024Review
- The Role of Trace Elements and Minerals in Osteoporosis: A Review of Epidemiological and Laboratory Findings.Biomolecules · 2023Review
- Hops extract and xanthohumol ameliorate bone loss induced by iron overload via activating Akt/GSK3β/Nrf2 pathway.Journal of bone and mineral metabolism · 2022Article
- Pentosan polysulfate regulates hepcidin 1-facilitated formation and function of osteoclast derived from canine bone marrow.PloS one · 2022Article
- Hepcidin contributes to Swedish mutant APP-induced osteoclastogenesis and trabecular bone loss.Bone research · 2021Article
- Ironing Out the Details: How Iron Orchestrates Macrophage Polarization.Frontiers in immunology · 2021Review
- Deletion of ferroportin in murine myeloid cells increases iron accumulation and stimulates osteoclastogenesisThe Journal of biological chemistry · 2018Article
- Biomarkers of inflammation and innate immunity in atrophic nonunion fracture.Journal of translational medicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepcidin is a key player in the regulation of mammalian iron homeostasis. Because iron overload may be one of the causes of osteoporosis, hepcidin may have therapeutic potential for osteoporosis patients. However, the effects of hepcidin on bone metabolism are not fully clear. We recently found that hepcidin can increase intracellular iron and calcium levels and promote mineralization in osteoblasts. The present study was designed to evaluate the effects of hepcidin on osteoclasts. Our results showed that mouse hepcidin 1 (MH1) can increase the number of TRAP-positive MNCs concomitant in both bone marrow-derived macrophages (BMMs) and RAW264.7 cells and upregulate mRNA levels of TRAP, cathepsin K, and MMP-9 and increase TRAP-5b protein secretion in RAW264.7 cells. Moreover, MH1 can downregulate the level of FPN1 protein and increase intracellular iron in RAW 264.7 cells. Therefore, we conclude that MH1 can significantly facilitate osteoclast differentiation in vitro. The mechanism behind accelerated differentiation may be associated with increased levels of intracellular iron. These findings may facilitate understanding of the effects of hepcidin on bone metabolism.
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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.