1.湖南中医药大学,长沙 410208
2.河南中医药大学 骨伤学院,郑州 450046
3.河南省洛阳正骨医院(河南省骨科医院),河南 洛阳 417002
张佳丽,在读硕士,从事中医药防治骨关节病方面的研究,E-mail:2725879412@qq.com
郭珈宜,硕士,教授,主任医师,博士生导师,从事中医药防治骨关节病方面的研究,E-mail:1184760535@qq.com
收稿:2026-03-17,
修回:2026-05-28,
录用:2026-06-03,
网络首发:2026-06-04,
纸质出版:2026-10-20
移动端阅览
张佳丽,张宇彬,宋若莹等.基于线粒体自噬从“虚气留滞”理论探讨原发性骨质疏松症的病机与治疗[J].中国实验方剂学杂志,2026,32(20):230-241.
ZHANG Jiali,ZHANG Yubin,SONG Ruoying,et al.Exploring Pathogenesis and Treatment of Primary Osteoporosis from Theory of Qi Deficiency and Stagnation and Mitochondrial Autophagy[J].Chinese Journal of Experimental Traditional Medical Formulae,2026,32(20):230-241.
张佳丽,张宇彬,宋若莹等.基于线粒体自噬从“虚气留滞”理论探讨原发性骨质疏松症的病机与治疗[J].中国实验方剂学杂志,2026,32(20):230-241. DOI: 10.13422/j.cnki.syfjx.20260713.
ZHANG Jiali,ZHANG Yubin,SONG Ruoying,et al.Exploring Pathogenesis and Treatment of Primary Osteoporosis from Theory of Qi Deficiency and Stagnation and Mitochondrial Autophagy[J].Chinese Journal of Experimental Traditional Medical Formulae,2026,32(20):230-241. DOI: 10.13422/j.cnki.syfjx.20260713.
原发性骨质疏松症(POP)是以骨量减少、骨微结构退化及骨脆性增加为特征的代谢性骨骼疾病,其发病机制涉及遗传、衰老、内分泌及环境等多种因素的交互作用,至今尚未完全阐明。线粒体功能障碍可引起三磷酸腺苷(ATP)生成不足及活性氧(ROS)异常堆积,激活氧化应激与炎症通路,进而抑制成骨细胞分化、促进破骨细胞活化,加剧POP的骨代谢负平衡。线粒体自噬作为线粒体质量控制的核心机制,能够选择性识别并清除受损线粒体,有效减少ROS堆积和能量代谢障碍,从而维持成骨-破骨细胞分化平衡。其在维持骨稳态及POP的预防与治疗中发挥关键作用。中医学“气化”功能与线粒体在能量生成及物质转化中的作用存在相似性;而“虚气留滞”的病理状态可能与线粒体自噬功能障碍相关联,“痰瘀互结”的致病特点亦与自噬流受阻诱发的代谢废物堆积有相通之处。该文基于“虚气留滞”理论,探讨其与线粒体自噬的相关性,并以此为切入点,阐释其在POP发病机制中的潜在作用。同时,结合POP“因虚致滞、虚实夹杂”的病机特点,提出基于“益气扶正、通络行滞”法从线粒体自噬视角论治POP的新思路,以期为进一步探索中医药防治POP提供理论支撑与研究启示。
Primary osteoporosis (POP) is a metabolic bone disease characterized by reduced bone mass, degenerated bone microstructure, and increased bone fragility. Its pathogenesis involves the interaction of multiple factors such as genetics, aging, endocrine, and environment, which remain incompletely elucidated. Mitochondrial dysfunction can lead to insufficient adenosine triphosphate (ATP) production and abnormal accumulation of reactive oxygen species (ROS), activating oxidative stress and inflammation pathways, thereby inhibiting osteoblast differentiation and promoting osteoclast activation, exacerbating the negative bone metabolism balance in POP. Mitochondrial autophagy, as the core mechanism of mitochondrial quality control, selectively identifies and clears damaged mitochondria to effectively reduce ROS accumulation and energy metabolism disorders, thus maintaining the balance between osteoblast and osteoclast differentiation. It plays a critical role in maintaining bone homeostasis and the prevention and treatment of POP. The traditional Chinese medicine (TCM) theory of Qi transformation shares similarities with the functions of mitochondria in energy generation and substance conversion. The pathological state of Qi deficiency and stagnation may be associated with mitochondrial autophagy dysfunction, and the pathogenic characteristics of combined phlegm and stasis align with the metabolic waste accumulation induced by obstructed autophagy flow. This article explores the correlation of the theory of Qi deficiency and stagnation with mitochondrial autophagy and elucidates its potential role in the pathogenesis of POP. Additionally, considering the pathogenesis features of POP, which involve deficiency causing stagnation and a mixture of deficiency and excess, this article proposes a novel therapeutic approach: tonifying Qi to support the body and unblocking collaterals to resolve stagnation from the perspective of mitochondrial autophagy. This article aims to provide theoretical support and research insights for further exploration of TCM in the prevention and treatment of POP.
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