骨形态发生蛋白介导的Smad依赖途径和Smad非依赖途径对骨质疏松症的潜在调节作用研究进展

王玉洁; 安方玉; 颜春鲁; 宋佳眙; 常伟荣; 张捷; 肖志攀; 高鹏; 李仲葓

引用本文:	王玉洁,安方玉,颜春鲁,宋佳眙,常伟荣,张捷,肖志攀,高鹏,李仲葓.骨形态发生蛋白介导的Smad依赖途径和Smad非依赖途径对骨质疏松症的潜在调节作用研究进展[J].中国现代应用药学,2024,41(2):277-286.
	WANG Yujie,AN Fangyu,YAN Chunlu,SONG Jiayi,CHANG Weirong,ZHANG Jie,XIAO Zhipan,GAO Peng,LI Zhonghong.Research Progress of Potential Regulatory Effects on Osteoporosis by BMP-mediated Smad Dependent and Smad Independent Pathways[J].Chin J Mod Appl Pharm(中国现代应用药学),2024,41(2):277-286.

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骨形态发生蛋白介导的Smad依赖途径和Smad非依赖途径对骨质疏松症的潜在调节作用研究进展
王玉洁¹, 安方玉^1,2, 颜春鲁^1,2,3, 宋佳眙¹, 常伟荣¹, 张捷¹, 肖志攀¹, 高鹏¹, 李仲葓¹
1.甘肃中医药大学, 兰州 730000;2.甘肃省高校重大疾病分子医学与中医药防治研究重点实验室, 兰州 730000;3.甘肃省中医药研究中心, 兰州 730000

摘要:

糖皮质激素长期使用、雌激素减少、继发性甲状旁腺功能亢进、骨组织微环境改变等多种因素均可诱发骨质疏松症。骨代谢失衡(成骨-成脂失衡)是骨质疏松症发病的关键机制，而骨髓间充质干细胞分化为脂肪细胞增加和成骨细胞减少是导致骨质疏松症成骨-成脂失衡的核心。骨形态发生蛋白(bone morphogenesis protein，BMP)则是调控骨质疏松症成骨-成脂平衡的关键蛋白，而这一调控作用又是通过Smad依赖途径和Smad非依赖途径来实现的。本文重点介绍了BMP介导的Smad依赖途径和Smad非依赖途径，并详细介绍了BMP-2、BMP-4、BMP-6、BMP-7、BMP-9通过上述途径参与骨质疏松症成骨、成脂代谢调控的可能机制，以期为临床抗骨质疏松症药物有效靶点的筛选提供新思路。

关键词: 骨质疏松症骨形态发生蛋白成骨分化成脂分化

DOI：10.13748/j.cnki.issn1007-7693.20231899

分类号:R966

基金项目:国家自然科学基金项目(82060872)；甘肃省自然科学基金项目(21JR11RA138)；兰州市科技计划项目资助(2022-3-22)；甘肃省“双一流”科研重点项目(GSSYLXM-05)；甘肃省高等学校创新基金项目(2022A-072)；甘肃省中医药管理局项目(GZKP-2023-39)

Research Progress of Potential Regulatory Effects on Osteoporosis by BMP-mediated Smad Dependent and Smad Independent Pathways

WANG Yujie¹, AN Fangyu^1,2, YAN Chunlu^1,2,3, SONG Jiayi¹, CHANG Weirong¹, ZHANG Jie¹, XIAO Zhipan¹, GAO Peng¹, LI Zhonghong¹

1.Gansu University of Traditional Chinese Medicine, Lanzhou 730000, China;2.Key Laboratory of Molecular Medicine and Chinese Medicine Prevention and Treatment of Major Diseases in Gansu Universities, Lanzhou 730000, China;3.Gansu Provincial Research Center of Traditional Chinese Medicine, Lanzhou 730000, China

Abstract:

Osteoporosis can be induced by various factors including prolonged glucocorticoid usage, diminished estrogen levels, secondary hyperparathyroidism, and alterations in the microenvironment of bone tissue. The bone metabolism imbalance(osteogenic-lipogenic imbalance) plays a crucial role in the development of osteoporosis. This imbalance is primarily driven by an increase in the differentiation of bone marrow mesenchymal stem cells into adipocytes and a decrease in their differentiation into osteoblasts, thus forming the core of the osteogenic-lipogenic imbalance observed in osteoporosis. The bone morphogenesis protein(BMP) plays a crucial role in the regulation of the osteogenic-lipid balance in osteoporosis. This regulatory function is accomplished through both the Smad-dependent and Smad-independent pathways. This review centers on the Smad-dependent and Smad-independent pathways facilitated by BMP, offering a comprehensive overview of the potential mechanisms through which BMP-2, 4, 6, 7, and 9 contribute to the regulation of osteogenesis and lipid metabolism in osteoporosis via these pathways. In order to present novel insights for the identification of efficacious targets for clinical anti-osteoporosis medications.

Key words: osteoporosis bone morphogenesis protein osteogenic differentiation adipogenic differentiation