Hepcidin-induced reduction in iron content and PGC-1β expression negatively regulates osteoclast differentiation to play a protective role in postmenopausal osteoporosis
Hui Zhang, Aifei Wang, Guangsi Shen, Xiao Wang, Gongwen Liu, Fan Yang, Bin Chen, Mingyong Wang, Youjia Xu
Abstract
. This study found that overexpression of hepcidin significantly inhibited ROS production, mitochondrial biogenesis, and PGC-1β expression. These data showed that hepcidin protected osteoporosis by reducing iron levels in bone tissue, and in conjunction with PGC-1β, reduced ROS production and the number of mitochondria, thus inhibiting osteoclast differentiation and bone absorption. Hepcidin could provide new targets for the clinical treatment of postmenopausal osteoporosis.
Topics & Concepts
HepcidinOsteoclastBone remodelingEndocrinologyOsteoporosisInternal medicineOsteoblastOvariectomized ratChemistryBone resorptionMitochondrial biogenesisDownregulation and upregulationMedicineMitochondrionEstrogenIn vitroInflammationBiochemistryReceptorGeneBone Metabolism and DiseasesCancer-related molecular mechanisms researchCancer, Lipids, and Metabolism