中国组织工程研究

中国组织工程研究 ›› 2026, Vol. 30 ›› Issue (23): 5982-5991.doi: 10.12307/2026.366

• 组织构建综述 tissue construction review • 上一篇    下一篇

线粒体自噬调控破骨细胞：骨质疏松症治疗的新视角

高佳斌1，李天奇1，徐  坤1，朱汉民1，周  茜2，李  微1   

  1. 1绍兴文理学院医学院，浙江省绍兴市   312099；2湖北文理学院基础医学院，湖北省襄阳市   441053
  • 收稿日期:2025-06-30 接受日期:2025-09-01 出版日期:2026-08-18 发布日期:2025-12-31
  • 通讯作者: 李微，博士，副教授，绍兴文理学院医学院，浙江省绍兴市 312099
  • 作者简介:高佳斌，男，2004年生，浙江省宁波市人，汉族，医学影像学专业本科在读。
  • 基金资助:
    国家自然科学基金青年项目(82205234)，项目负责人：李微；湖北省自然科学基金联合基金项目(2024AFD049)，项目负责人：周茜；襄阳市科技局重点项目(2022YL07A)，项目负责人：李微；浙江省医学会临床医学专项基金项目(2023ZYC-A182)，项目负责人：李微；绍兴文理学院校级科研项目重点项目(2024LG011)，项目负责人：朱汉民；绍兴文理学院科研启动金项目，项目负责人：李微；绍兴市基础公益专项项目(2025A14022)，项目负责人：李微

Mitophagy regulates osteoclasts: a new perspective for osteoporosis treatment

Gao Jiabin1, Li Tianqi1, Xu Kun1, Zhu Hanmin1, Zhou Xi2, Li Wei1   

  1. 1Medicine College, Shaoxing University, Shaoxing 312099, Zhejiang Province, China; 2Basic Medical College, Hubei University of Arts and Sciences, Xiangyang 441053, Hubei Province, China
  • Received:2025-06-30 Accepted:2025-09-01 Online:2026-08-18 Published:2025-12-31
  • Contact: Li Wei, PhD, Associate professor, Medicine College, Shaoxing University, Shaoxing 312099, Zhejiang Province, China
  • About author:Gao Jiabin, Medicine College, Shaoxing University, Shaoxing 312099, Zhejiang Province, China
  • Supported by:
    National Natural Science Foundation of China (Youth Program), No. 82205234 (to LW); Hubei Provincial Natural Science Foundation Joint Fund Project, No. 2024AFD049 (to ZX); Xiangyang Municipal Science and Technology Bureau Key Project, No. 2022YL07A (to LW); Zhejiang Medical Association Clinical Medicine Special Fund Project, No. 2023ZYC-A182 (to LW); Shaoxing University Key Research Project, No. 2024LG011 (to ZHM); Shaoxing University Research Start-up Fund Project (to LW); Shaoxing Municipal Basic Public Welfare Special Project, No. 2025A14022 (to LW)

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摘要：



文题释义：
破骨细胞：是维持骨稳态过程不可或缺的一种细胞，主要参与骨吸收过程。破骨细胞分泌的一些因子也会影响到成骨细胞功能，因此，调节破骨细胞的功能是改善骨代谢的一种非常重要的途径。
线粒体自噬：是细胞内一种关键的线粒体质量控制机制，主要功能是选择性地清除损伤或功能紊乱的线粒体。线粒体自噬主要的途径有同源性磷酸酶张力蛋白诱导的激酶/E3泛素连接酶途径和受体介导的线粒体自噬途径。

背景：骨质疏松症的发生与骨稳态失衡密切相关，尤其是破骨细胞的骨吸收作用增强。线粒体自噬作为一种选择性清除受损线粒体的自噬途径，近年来被发现与骨质疏松症的发生发展密切相关。
目的：综述线粒体自噬的机制及其在破骨细胞中的调控作用，探讨线粒体自噬通过调控破骨细胞的形成、凋亡等功能影响骨稳态的潜在机制。
方法：检索PubMed、中国知网、万方和维普数据库2008年1月至2025年4月发表的相关文献，中文关键词为“线粒体自噬，骨代谢，破骨细胞，骨稳态，骨吸收，骨丢失”，英文关键词为“Mitophagy，Bone Metabolism，Osteoclasts，Bone homeostasis，bone resorption，bone loss”，依据入选标准对检索结果进行筛选，最终纳入101篇文献进行综述分析。
结果与结论：线粒体自噬是细胞内一种关键的线粒体质量控制机制，主要功能是选择性地清除损伤或功能紊乱的线粒体。线粒体自噬主要的途径有同源性磷酸酶张力蛋白诱导的激酶/E3泛素连接酶途径和受体介导的线粒体自噬途径。线粒体自噬在机体中往往表现出有利和有害的双重性质。线粒体自噬过激可以通过维持胞内活性氧稳态、调节能量代谢、促进破骨细胞分化和抑制破骨细胞凋亡诱发骨吸收增加，进而导致骨代谢失衡，发生骨质疏松症。
https://orcid.org/0009-0005-2031-5442 (高佳斌)


中国组织工程研究杂志出版内容重点：干细胞；骨髓干细胞；造血干细胞；脂肪干细胞；肿瘤干细胞；胚胎干细胞；脐带脐血干细胞；干细胞诱导；干细胞分化；组织工程

关键词: 线粒体自噬, 骨质疏松症, 破骨细胞, 骨稳态, 骨代谢, 骨吸收, 组织构建

Abstract: BACKGROUND: The development of osteoporosis is closely associated with the disruption of bone homeostasis, particularly due to the enhanced bone resorption activity of osteoclasts. Mitophagy, an autophagic pathway that selectively degrades damaged mitochondria, has recently been identified as being intricately linked to the pathogenesis and progression of osteoporosis.
OBJECTIVE: To elucidate the mechanisms of mitophagy and its regulatory roles in osteoclasts and to investigate the potential mechanisms by which mitophagy influences bone homeostasis through the regulation of osteoclastogenesis and apoptosis.
METHODS: The databases searched included PubMed, CNKI, WanFang Data, and VIP databases. The search terms were “mitophagy, bone metabolism, osteoclasts, bone homeostasis, bone resorption, bone loss” in Chinese and English. The search time frame was from January 2008 to April 2025. Based on the inclusion criteria, the search results were screened and excluded, and 101 articles were finally included for review and analysis.
RESULTS AND CONCLUTION: Mitophagy is a crucial mitochondrial quality control mechanism within cells, primarily responsible for the selective elimination of damaged or dysfunctional mitochondria. The main pathways of mitophagy include the phosphatase and tensin homolog-induced kinase 1/E3 ubiquitin ligase pathway and the receptor-mediated mitophagy pathway. Mitophagy often exhibits dual beneficial and detrimental properties in the body. Excessive mitophagy can lead to imbalance of bone metabolism and subsequent osteoporosis by maintaining intracellular reactive oxygen species homeostasis, regulating energy metabolism, promoting osteoclast differentiation, inhibiting osteoclast apoptosis, and increasing bone resorption. 

Key words: mitophagy, osteoporosis, osteoclasts, bone homeostasis, bone metabolism, bone resorption, tissue construction

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