上海交通大学学报(医学版) ›› 2023, Vol. 43 ›› Issue (6): 761-767.doi: 10.3969/j.issn.1674-8115.2023.06.013

• 综述 • 上一篇    

线粒体功能障碍与骨质疏松症相关性研究进展

金芳全1(), 樊成虎2, 唐晓栋2(), 陈彦同2, 齐兵献2   

  1. 1.甘肃中医药大学中医临床学院,兰州 730030
    2.甘肃省中医院脊柱中心,兰州 730050
  • 收稿日期:2023-02-08 接受日期:2023-06-21 出版日期:2023-06-28 发布日期:2023-06-28
  • 通讯作者: 唐晓栋 E-mail:3214555282@qq.com;1927981689@qq.com
  • 作者简介:金芳全(1994—),男,硕士生,电子信箱:3214555282@qq.com
  • 基金资助:
    国家自然科学基金(81760877);甘肃省科技厅重点研发计划社会发展类项目(21ZD4FA009);甘肃省中医药重点课题(GZKZ-2021-3);甘肃省中医药科研课题(GZKP-2021-12)

Research progress in the relationship between mitochondrial dysfunction and osteoporosis

JIN Fangquan1(), FAN Chenghu2, TANG Xiaodong2(), CHEN Yantong2, QI Bingxian2   

  1. 1.Clinical College of Chinese Medicine, Gansu University of Traditional Chinese Medicine, Lanzhou 730030
    2.Gansu Provincial Hospital of Traditional Chinese Medicine Spine Center, Lanzhou 730050
  • Received:2023-02-08 Accepted:2023-06-21 Online:2023-06-28 Published:2023-06-28
  • Contact: TANG Xiaodong E-mail:3214555282@qq.com;1927981689@qq.com
  • Supported by:
    National Natural Science Foundation of China(81760877);Social Development Project of Key Research and Development Program of Gansu Provincial Department of Science and Technology(21ZD4FA009);Key Project of Traditional Chinese Medicine of Gansu Province(GZKZ-2021-3);Scientific Research Project of Traditional Chinese Medicine of Gansu Province(GZKP-2021-12)

摘要:

骨质疏松症(osteoporosis,OP)是一种以骨量减少、骨脆性增加为特征的慢性老年性骨病,诱发因素较多且发病机制复杂。探究OP机制,提高临床疗效一直是生命科学领域的研究热点。近年来研究发现线粒体在OP发病机制中具有重要意义。线粒体能量代谢、线粒体氧化应激、线粒体自噬、线粒体介导的凋亡、线粒体动力学等功能异常均可通过不同信号通路、细胞因子及蛋白质表达干预骨髓间充质干细胞分化命运,调控成骨细胞活性及增殖分化,启动破骨细胞凋亡程序。因此以线粒体为靶点,调节线粒体能量代谢、氧化应激、自噬、动力学等功能,诱导骨髓间充质干细胞成骨分化,促进成骨细胞分化与矿化,诱导破骨细胞凋亡是防治OP的潜在策略。该文查阅国内外相关文献,就线粒体功能障碍在OP中的作用机制作一综述,以期为进一步研究奠定基础。

关键词: 线粒体, 骨质疏松症, 氧化应激, 自噬, 线粒体动力学

Abstract:

Osteoporosis (OP) is a chronic senile bone disease characterized by decreased bone mass and increased bone fragility. There are many inducing factors and the pathogenesis is complex. To explore the mechanism of OP and improve clinical efficacy has always been a hot topic in life science. In recent years, it has been found that mitochondria play an important role in the pathogenesis of OP. Functional abnormalities such as mitochondrial energy metabolism, mitochondrial oxidative stress, mitochondrial autophagy, mitochondrial-mediated apoptosis and mitochondrial dynamics can interfere with the differentiation of bone marrow mesenchymal stem cells through different signal pathways, cytokines and protein expression to regulate osteoblast activity, proliferation and differentiation, and start the process of osteoclast apoptosis. Therefore, taking mitochondria as the target, regulating the functions of mitochondrial energy metabolism, oxidative stress, autophagy and kinetics, inducing osteogenic differentiation of bone marrow mesenchymal stem cells, promoting osteoblast differentiation and mineralization, and inducing osteoclast apoptosis are potential strategies for the prevention and treatment of OP. In this article, the mechanism of mitochondrial dysfunction in OP was reviewed by referring to relevant literature at home and abroad, in order to lay a foundation for further research.

Key words: mitochondria, osteoporosis, oxidative stress, autophagy, mitochondrial dynamics

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