CAJ | 학술논문

绝经后妇女因为体内雌激素活性的降低，发生骨质疏松及骨折的风险显著增加，但雌激素抑制骨质疏松的作用机制长期以来并不明了。近年来，随着基因敲除等分子生物学技术的飞速发展，通过分别敲除小鼠体内不同骨细胞中的雌激素受体α（estrogen receptorα，ERα），逐渐揭示了ERα在雌激素与骨质疏松关系中的重要作用，对研发预防及治疗骨质疏松药物等具有重要的临床意义。由不同骨细胞中ERα对骨代谢的作用入手，分别分析阐明骨细胞、破骨细胞、成骨细胞祖细胞、成熟成骨细胞与骨细胞中的ERα在骨质疏松发病机制中的作用，对于开发骨质疏松药物的新靶点具有十分重要的意义。
절경후부녀인위체내자격소활성적강저，발생골질소송급골절적풍험현저증가，단자격소억제골질소송적작용궤제장기이래병불명료。근년래，수착기인고제등분자생물학기술적비속발전，통과분별고제소서체내불동골세포중적자격소수체α（estrogen receptorα，ERα），축점게시료ERα재자격소여골질소송관계중적중요작용，대연발예방급치료골질소송약물등구유중요적림상의의。유불동골세포중ERα대골대사적작용입수，분별분석천명골세포、파골세포、성골세포조세포、성숙성골세포여골세포중적ERα재골질소송발병궤제중적작용，대우개발골질소송약물적신파점구유십분중요적의의。
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.