Article(id=1291704844516086356, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704811443999077, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.18.020, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1740844800000, receivedDateStr=2025-03-02, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896033646, onlineDateStr=2026-08-05, pubDate=1758988800000, pubDateStr=2025-09-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896033646, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896033646, creator=13701087609, updateTime=1785896033646, updator=13701087609, issue=Issue{id=1291704811443999077, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='18', pageStart='2551', pageEnd='2700', issueExtLink='null', onlineDate='null', pubDate='1758988800000', pubDateStr='2025-09-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896025763, creator='13701087609', updateTime=1785896871490, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291708358743053253, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704811443999077, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291708358743053254, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704811443999077, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2685, endPage=2691, ext={EN=ArticleExt(id=1291704844721607253, articleId=1291704844516086356, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research status of regulatory mechanism of mitochondrial autophagy in osteoarthritis and intervention of traditional Chinese medicine, columnId=1246531408630534361, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Osteoarthritis, a degenerative bone disease commonly seen in the elderly, is particularly prevalent in weight-bearing joints such as the knee. Its etiology is multifactorial and characterized by pathological changes in the joint structure, including destruction and degeneration of articular cartilage, inflammatory response and formation of bone capillaries. Up to now, clinical treatment for osteoarthritis is mainly symptomatic treatment and pain relief, and there is no exact therapy that can reverse the pathological process of cartilage damage in osteoarthritis. In recent years, domestic and foreign scholars have found that mitochondria, as important organelles of chondrocytes, plays an important role in the process of cell metabolism, proliferation and apoptosis. It is also pointed out that mitochondrial autophagy imbalance is an important factor leading to cartilage damage in joints. Meanwhile, several basic experiments have shown that Chinese medicine exhibits the potential to protect cartilage by targeting the regulation of mitochondrial autophagy, thus showing positive results in the prevention and treatment of osteoarthritis. However, studies on this area have not been systematically elaborated. In view of this, the authors will systematically elaborate on the effects of mitochondrial autophagy on the development of osteoarthritis and the role of TCM in interfering with mitochondrial autophagy in the treatment of osteoarthritis, with the aim of providing new ideas and methods for the development of new medicines and therapeutic strategies for the treatment of osteoarthritis with TCM.

, authors=Xun-ru ZHANG¹, Hong-zhuan LI², Fei WANG¹, Zong-yang CHEN¹, Jia-qi LIANG¹, Li-peng WEN¹, Zhong-feng LI², authorsList=Xun-ru ZHANG, Hong-zhuan LI, Fei WANG, Zong-yang CHEN, Jia-qi LIANG, Li-peng WEN, Zhong-feng LI, authorCompany=null, correspAuthors=Hong-zhuan LI, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291704845090706006, articleId=1291704844516086356, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=线粒体自噬在骨性关节炎中的调控机制及中医药干预研究进展, columnId=1246531408819278046, journalTitle=中国临床药理学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

骨性关节炎作为一种常见于老年人的退行性骨病，尤其好发于负重关节如膝关节。其病因是多因素的，特点是关节结构发生病理变化，包括关节软骨的破坏和退化、炎症反应以及骨赘的形成。截至目前，临床上对于骨性关节炎的治疗主要是对症治疗和缓解疼痛，尚无确切疗法能够逆转骨性关节炎中软骨损伤的病理进程。而近年来，国内外学者研究发现，线粒体作为软骨细胞重要的细胞器，在细胞的代谢、增殖和凋亡过程中扮演着重要角色。研究还指出，线粒体自噬失衡是导致关节内软骨损伤的一个重要因素。与此同时，多项基础实验表明，中医药通过靶向调节线粒体自噬，展现出保护软骨的潜力，从而在防治骨性关节炎方面显示出积极效果。然而，关于这一领域的研究尚未得到系统性的阐述。鉴于此，笔者将从线粒体自噬对骨性关节炎发生发展的影响及中医药干预线粒体自噬治疗骨性关节炎的作用进行系统性阐述，以期为中医药治疗骨性关节炎的新药研发及治疗策略提供新的思路和方法。

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张循儒（1997-），男，硕士研究生，主要从事中医药治疗骨伤病的研究

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张循儒（1997-），男，硕士研究生，主要从事中医药治疗骨伤病的研究

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