摘要
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。
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.
出处
《国际妇产科学杂志》
CAS
2014年第6期636-638,共3页
Journal of International Obstetrics and Gynecology