Journal
JOURNAL OF MOLECULAR ENDOCRINOLOGY
Volume 60, Issue 4, Pages 299-308Publisher
BIOSCIENTIFICA LTD
DOI: 10.1530/JME-17-0301
Keywords
hepcidin; osteoporosis; oxidative stress; bone metabolism; iron metabolism
Categories
Funding
- National Natural Science Foundation of China [81502812, 81572179, 81773439]
- Clinical Special Program of Jiangsu Province [BL2014044]
- Minsheng Science and Technology Project of Suzhou [SS201634]
- Clinical Medical Center Project of Suzhou [Szzx201504]
- Advantage Discipline Groups of the Second Affiliated Hospital of Soochow University [XKQ2015001]
Ask authors/readers for more resources
Postmenopausal osteoporosis is a global health issue. Although a lack of estrogen is considered the major reason for postmenopausal osteoporosis, other factors might also contribute the etiology of the disease. In previous reports, we and others proposed that iron accumulation after menopause accelerates osteoporosis, and here, we genetically modified the expression of an endogenous hormone, hepcidin, to modulate iron status in a mouse model. Our results show that hepcidin levels negatively correlate with bone loss in both knockout and overexpression (with ovariectomy) murine models. In addition, iron overload enhances reactive oxygen species (ROS) activity and attenuates the functions of primary osteoblasts, while iron depletion could reverse this phenomenon through inhibiting the functions of primary osteoclasts. Therefore, our results provide more evidence of the 'iron accumulation' hypothesis, which suggests that high iron levels are risk factors for osteoporosis, and the 'Huang's hypothesis' that hepcidin is a potential drug target for the prevention of postmenopausal osteoporosis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available