{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T16:06:52Z","timestamp":1791994012492,"version":"4.4.0"},"reference-count":74,"publisher":"Bioscientifica","issue":"4","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2018,5]]},"abstract":"<jats:p>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 \u2018iron accumulation\u2019 hypothesis, which suggests that high iron levels are risk factors for osteoporosis, and the \u2018Huang\u2019s hypothesis\u2019 that hepcidin is a potential drug target for the prevention of postmenopausal osteoporosis.<\/jats:p>","DOI":"10.1530\/jme-17-0301","type":"journal-article","created":{"date-parts":[[2018,3,21]],"date-time":"2018-03-21T12:50:24Z","timestamp":1521636624000},"page":"299-308","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-6","source":"Crossref","is-referenced-by-count":32,"title":["Hepcidin is an endogenous protective factor for osteoporosis by reducing iron levels"],"prefix":"10.1530","volume":"60","author":[{"given":"Peng","family":"Zhang","sequence":"first","affiliation":[{"name":"1Department of Orthopaedics, the Second Affiliated Hospital of Soochow University, Suzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sheng","family":"Wang","sequence":"additional","affiliation":[{"name":"2Emergency Department, Zhongshan Hospital Affiliated to Fudan University, Shanghai, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liang","family":"Wang","sequence":"additional","affiliation":[{"name":"3Department of Radiology, Children's Hospital of Soochow University, Suzhou, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bing Chen","family":"Shan","sequence":"additional","affiliation":[{"name":"1Department of Orthopaedics, the Second Affiliated Hospital of Soochow University, Suzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Zhang","sequence":"additional","affiliation":[{"name":"4Osteoprosis Institute of Soochow University, Suzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fan","family":"Yang","sequence":"additional","affiliation":[{"name":"4Osteoprosis Institute of Soochow University, Suzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhi Qiang","family":"Zhou","sequence":"additional","affiliation":[{"name":"1Department of Orthopaedics, the Second Affiliated Hospital of Soochow University, Suzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao","family":"Wang","sequence":"additional","affiliation":[{"name":"4Osteoprosis Institute of Soochow University, Suzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ye","family":"Yuan","sequence":"additional","affiliation":[{"name":"4Osteoprosis Institute of Soochow University, Suzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"You Jia","family":"Xu","sequence":"additional","affiliation":[{"name":"1Department of Orthopaedics, the Second 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