期刊
GENE
卷 543, 期 1, 页码 161-165出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.gene.2014.02.023
关键词
Hepcidin deficiency; Iron overload; Bone resorption; Bone strength
资金
- national 973 program [2014CB932000]
- National Natural Science Foundation of China [21377159]
Osteoporosis is one of the leading disorders among aged people. Bone loss results from a number of physiological alterations, such as estrogen decline and aging. Meanwhile, iron overload has been recognized as a risk factor for bone loss. Systemic iron homeostasis is fundamentally governed by the hepcidin-ferroportin regulatory axis, where hepcidin is the key regulator. Hepcidin deficiency could induce a few disorders, of which iron overload is the most representative phenotype. However, there was little investigation of the effects of hepcidin deficiency on bone metabolism. To this end, hepcidin-deficient (Hamp1(-/-)) mice were employed to address this issue. Our results revealed that significant iron overload was induced in Hamp1(-/-) mice. Importantly, significant decreases of maximal loading and maximal bending stress were found in Hamp1(-/-) mice relative to wildtype (WT) mice. Moreover, the levels of the C-telopeptide of type I collagen (CTX-1) increased in Hamp1(-/-) mice. Therefore, hepcidin deficiency resulted in a marked reduction of bone load-bearing capacity likely through enhancing bone resorption, suggesting a direct correlation between hepcidin deficiency and bone loss Targeting hepcidin or the pathway it modulates may thus represent a therapeutic for osteopenia or osteoporosis. (C) 2014 Elsevier B.V. All rights reserved.
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