Article(id=1291707009955549235, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.21.022, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1754755200000, receivedDateStr=2025-08-10, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896549928, onlineDateStr=2026-08-05, pubDate=1763308800000, pubDateStr=2025-11-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896549928, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896549928, creator=13701087609, updateTime=1785896549928, updator=13701087609, issue=Issue{id=1291706987964822180, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='21', pageStart='3001', pageEnd='3150', issueExtLink='null', onlineDate='null', pubDate='1763308800000', pubDateStr='2025-11-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896544684, creator='13701087609', updateTime=1785896721343, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291707729324826977, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291707729324826978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291706987964822180, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=3132, endPage=3138, ext={EN=ArticleExt(id=1291707010198818868, articleId=1291707009955549235, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research progress of role of natural compounds in regulating GPX4 in osteoarthritis pathogenesis, columnId=1246531408630534361, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Osteoarthritis (OA) is a common chronic degenerative joint disease, primarily characterized by cartilage wear, degeneration and inflammatory responses. The pathological mechanisms mainly involve excessive reactive oxygen species (ROS) production in synovial membranes causing oxidative stress, pro-inflammatory factors inducing inflammation and cartilage cell death. Ferroptosis, a distinct form of cellular death different from autophagy and apoptosis, has been shown to accelerate OA progression through iron deposition and lipid peroxidation. Enhanced lipid peroxidation and oxidative stress in OA-affected cartilage cells, combined with increased inflammatory responses, exacerbate cartilage damage. Glutathione peroxidase 4 (GPX4), an antioxidant enzyme, inhibits oxidative stress to prevent ferroptosis and slow OA progression. Traditional Chinese medicinal (TCM) natural products have gained prominence due to their unique therapeutic effects and broad-spectrum applications. These compounds have demonstrated antioxidant and anti-inflammatory properties against various diseases, thereby delaying OA progression. This research progress aims to investigate how TCM natural products regulate the GPX4 signaling pathway to mitigate cartilage cell ferroptosis and its impact on OA, exploring potential mechanisms that may provide novel strategies for clinical prevention and treatment of OA.

, authors=Ni HA¹, Zi-ming JIN^{1, 2}, Hao-fei YANG², Xia DOU^{1, 2}, Wei-li MA¹, Jin-sheng LI², Xu-dong ZHU², Jian-rong ZHANG², authorsList=Ni HA, Zi-ming JIN, Hao-fei YANG, Xia DOU, Wei-li MA, Jin-sheng LI, Xu-dong ZHU, Jian-rong ZHANG, authorCompany=null, correspAuthors=Zi-ming JIN, 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=1291707010463060021, articleId=1291707009955549235, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=中药天然产物调控GPX4在骨性关节炎中的发病机制及研究进展, 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（OA）是一种常见的慢性退行性关节疾病，主要病理改变以关节软骨磨损、退变、炎症反应为主。病理机制主要由关节滑膜产生过多活性氧导致氧化应激、促炎因子产生炎症和软骨细胞死亡所导致。铁死亡是一种与细胞自噬、凋亡不同的细胞死亡类型，研究表明，软骨细胞铁死亡加速骨关节炎的发展，铁死亡主要通过铁沉积与脂质过氧化引起，通过加重OA的软骨细胞中脂质过氧化及氧化应激、炎症反应增加软骨损伤。谷胱甘肽过氧化物酶4（GPX4）是一种抗氧化产物，其通过抑制氧化应激来阻止铁死亡的发生，减轻OA的进展。中药天然产物因其独特的疗效与广泛的治疗作用而突出，且已被证明在多种疾病中具有抗氧化和抗炎特性，从而延缓OA进展。因此，本文旨在确定中药天然产物通过调控GPX4信号通路减轻软骨细胞铁死亡及其对OA的影响以及潜在的机制，为临床防治OA的发生发展提供新的思路及策略。

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哈妮（1988－），女，主管药师，主要从事中药防治慢性疾病的相关研究

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哈妮（1988－），女，主管药师，主要从事中药防治慢性疾病的相关研究

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