| First Author | Shen GS | Year | 2014 |
| Journal | Calcif Tissue Int | Volume | 94 |
| Issue | 6 | Pages | 632-9 |
| PubMed ID | 24652331 | Mgi Jnum | J:319351 |
| Mgi Id | MGI:6862549 | Doi | 10.1007/s00223-014-9845-8 |
| Citation | Shen GS, et al. (2014) Hepcidin1 knockout mice display defects in bone microarchitecture and changes of bone formation markers. Calcif Tissue Int 94(6):632-9 |
| abstractText | Iron accumulation is a risk factor of osteoporosis; mechanisms leading to iron-related bone loss are not fully determined. We sought to better understand the effect of chronic iron accumulation on bone over the life span in a mouse model. Hepcidin1 knockout (Hepc1(-/-)) male mice and their littermate control wild type (WT) mice at 7 months old were used in this study. Serum iron and ferritin as well as iron contents in liver and femur were significantly increased in Hepc1(-/-) mice compared to WT mice. We found that Hepc1(-/-) mice had a phenotype of low bone mass and alteration of the bone microarchitecture, most likely caused by a decreased osteoblastic activity. Cell culture studies indicated that chronic iron accumulation decreased bone formation, probably by affecting bone morphogenetic protein signaling. |
