本文系统总结了滑膜细胞衰老在骨关节炎（OA）发生发展中的核心病理机制，并聚焦近年来针对衰老滑膜细胞的靶向治疗进展，以期为OA的精准干预提供理论依据。通过检索近年PubMed、Web of Science及中国知网数据库相关文献，分析了滑膜细胞衰老的分子机制及其通过衰老相关分泌表型（SASP）介导的病理效应。研究发现，衰老滑膜细胞通过释放促炎因子及基质降解酶，驱动滑膜慢性炎症、软骨退变及关节功能丧失。近年来，senolytics药物（如D+Q联合疗法）、CRISPR基因编辑技术及间充质干细胞移植等新兴手段在清除衰老滑膜细胞或逆转其病理表型方面显示出显著疗效，可有效改善OA动物模型的关节损伤。靶向滑膜细胞衰老的干预策略为OA治疗开辟了新的方向，未来亟需进一步阐明衰老微环境的时空动态变化，并推动相关成果的临床转化。

This review systematically summarized the core pathological mechanisms of synovial cell senescence in the onset and progression of osteoarthritis (OA) and focused on recent advances in targeted therapies for senescent synovial cells, aiming to provide a theoretical basis for precise OA interventions. Relevant literature from PubMed, Web of Science, and China National Knowledge Infrastructure (CNKI) databases in recent years was reviewed to analyze the molecular mechanisms of synovial cell senescence and its pathological effects mediated by the senescence-associated secretory phenotype (SASP). The findings indicate that senescent synovial cells release pro-inflammatory cytokines and matrix-degrading enzymes (e.g., MMP-13), which drive chronic synovial inflammation, cartilage degeneration, and loss of joint function. In recent years, emerging approaches such as senolytic drugs (e.g., dasatinib plus quercetin combination therapy), CRISPR-based gene editing, and mesenchymal stem cell transplantation have shown significant efficacy in eliminating senescent synovial cells or reversing their pathological phenotype, thereby ameliorating joint damage in OA animal models. Targeting synovial cell senescence offers a novel direction for OA treatment, and future studies are urgently needed to further elucidate the spatiotemporal dynamics of the senescent microenvironment and facilitate the clinical translation of these findings.