摘要
Abstract
Reduced bioavailability of estrogen increases osteoporosis and fracture risk in postmenopausal women significantly,but the mechanisms by which estrogen regulates bone mass are incompletely understood. In recent years ,mouse models with cell-specific deletion of the estrogen receptorα (ERα) have provided novel insights into the function and signaling of ERαwhich provide opportunity to develop new drugs for preventing and treating osteoporosis. Illuminating the role of ERαin different bone cells,including chondrocyte,osteoclast,osteoblast progenitor cells,osteoblast and osteocyte to figure out the mechanisms of ERαin the pathogenesis of osteoporosis is of great importance to find new targets for osteoporosis.关键词
雌激素受体α/骨质疏松/骨质疏松,绝经后/绝经后期/小鼠,基因敲除Key words
Estrogen receptor alpha/Osteoporosis/Osteoporosis,postmenopausal/Postmenopause/Mice,knockout
