利用间充质干细胞（mesenchymal stem cells, MSCs）修复组织损伤对提高骨关节炎（osteoarthritis, OA）疾病治疗水平意义重大。本文前期研究发现，人MSC来源的外泌体中lncRNA KLF3-AS1能促进软骨细胞增殖、抑制软骨细胞凋亡，缓解OA的发生、发展。进一步预实验显示，lncRNA KLF3-AS1和YBX1之间确实存在结合关系；此外，干扰lncRNA KLF3-AS1下调PI3K/Akt/mTOR信号通路，促进软骨细胞自噬和凋亡。因此，我们提出：人MSC来源的外泌体中lncRNA KLF3-AS1通过结合转录因子YBX1，激活PI3K/Akt/mTOR信号通路，抑制软骨细胞自噬，减少细胞凋亡，最终修复OA导致的软骨组织损伤。该研究可能阐明了外泌体中lncRNA KLF3-AS1对软骨组织修复的分子机制，为软骨组织损伤治疗提供新的方法。

It was well documented that mesenchymal stem cells (MSCs) played an important role in the repair of the injured cartilage for treatment of osteoarthritis (OA). Our preliminary research showed that exosomal lncRNA KLF3-AS1 from hMSCs could promote proliferation and inhibit apoptosis of chondrocytes, which in turn relieve the occurrence and development of OA. Further experiments revealed that lncRNA KLF3-AS1 interacted with Y-box binding protein-1 (YBX1). Additionally, miR-135b expression levels were significantly increased in rat MSC-exosome stimulated by TGF-β1. Furthermore, lncRNA KLF3-AS1 knockdown downregulated PI3K/Akt/mTOR signaling pathway, leading to increased chondrocyte autophagy and apoptosis. As a result, we speculated that exosomal lncRNA KLF3-AS1 from hMSCs inhibited chondrocyte autophagy and apoptosis through PI3K/Akt/mTOR activation by interacting with YBX1, thereby alleviating OA-induced cartilage injury. In this study, we aimed to reveal the molecular mechanisms of exosomal lncRNA KLF3-AS1 from hMSCs on the repair of cartilage defects, providing a new method for cartilage injury treatment.