Article(id=1291753215788339806, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, articleNumber=PA20260408_Cl2GceP9, orderNo=null, doi=10.3969/j.issn.1671-7856.2026.06.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1755100800000, receivedDateStr=2025-08-14, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785907566259, onlineDateStr=2026-08-05, pubDate=1774800000000, pubDateStr=2026-03-30, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785907566258, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785907566258, creator=admin, updateTime=1785907566258, updator=admin, issue=Issue{id=1291753151179280707, tenantId=1146029695717560320, journalId=1291416913693474840, year='2026', volume='36', issue='6', pageStart='1', pageEnd='144', issueExtLink='null', onlineDate='null', pubDate='1774800000000', pubDateStr='2026-03-30', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1785907550854, creator='ztmeta', updateTime=1786331902788, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1293533012289941791, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1293533012289941792, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=90, endPage=101, ext={EN=ArticleExt(id=1291753220183970400, articleId=1291753215788339806, tenantId=1146029695717560320, journalId=1291416913693474840, language=EN, title=Research progress on lactylation modification in osteoarticular degenerative diseases, columnId=1292760404241969391, journalTitle=Chinese Journal of Comparative Medicine, columnName=Research Progress, runingTitle=null, highlight=null, articleAbstract=

Post-translational modifications (PTMs) are crucial for regulating protein functions. As a novel PTM, lactylation has emerged as a recent research hotspot, participating in pathological processes such as tumor progression and inflammation; it dynamically regulates gene expression and protein activity, which is significant for metabolic-immune coordination. In degenerative osteoarthropathy (such as osteoarthritis and rheumatoid arthritis), cartilage metabolic imbalance is closely associated with dynamic changes in lactylation, involving pathological links such as cartilage matrix degradation, synovial inflammation, and abnormal bone remodeling. Current clinical interventions cannot block disease progression. This review systematically summarizes the molecular mechanisms of lactylation (including lactate metabolism as well as histone and non-histone lactylation), regulatory factors (enzymes, environment, and molecular tools), and its role in degenerative osteoarthropathy, covering expression changes in cartilage tissues, correlation with arthritis progression, and biomarker studies in clinical models. Lactylation affects joint degeneration by regulating glycolysis-oxidative phosphorylation balance, inflammatory factor expression, and extracellular matrix metabolism. Targeted regulation strategies (such as CRISPR editing and small-molecule inhibitors) hold promise as novel therapeutic approaches. Future research needs to overcome technical limitations in detection, decipher the dynamic lactylation network through interdisciplinary collaboration, and promote its clinical translation in early diagnosis, precise intervention, and personalized treatment.

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蛋白质翻译后修饰（PTMs）是调控蛋白质功能的重要机制，乳酸化修饰作为一种新兴的PTM类型，近年来逐渐成为研究热点。其通过动态调控基因表达和蛋白活性参与肿瘤、炎症等病理过程，在代谢-免疫协同调控中具有重要作用。在骨关节退变性疾病（如骨关节炎或椎间盘退变性疾病等）中，软骨组织代谢失衡与乳酸化修饰动态变化密切相关，涉及基质降解、滑膜炎症及骨重塑异常等病理环节，但现有临床干预手段无法阻断疾病进展。本文系统综述乳酸化修饰的分子机制（包括乳酸代谢、组蛋白与非组蛋白乳酸化）、调控因素（酶、环境、分子工具）及其在骨关节退变性疾病中的研究进展，涵盖软骨组织表达变化、与疾病进展的关联及临床模型中的标记物研究。结果表明，乳酸化修饰通过调控糖酵解-氧化磷酸化平衡、炎症因子表达及细胞外基质代谢影响骨关节退变，针对乳酸化修饰的靶向调控（如CRISPR编辑、小分子抑制剂）有望成为骨关节退变性疾病的新型治疗策略。未来需突破检测技术瓶颈，通过跨学科合作解析乳酸化动态网络，推动其在早期诊断、精准干预及个性化治疗中的临床转化。

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侯承钰（2002—），男，在读硕士研究生，研究方向：骨科。E-mail: 1816234515@qq.com

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侯承钰（2002—），男，在读硕士研究生，研究方向：骨科。E-mail: 1816234515@qq.com

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