软骨细胞衰老是骨关节炎（OA）的重要致病机制。已有动物实验表明抑制软骨细胞衰老可以延缓OA，但具体调控机制仍不明确。而环状RNA在OA发生发展中发挥重要作用，但在软骨细胞衰老方面鲜有报道。我们发现，在人OA软骨细胞中，环状RNA CircSLC39A8表达下降，而在人软骨细胞中沉默CircSLC39A8可以诱导软骨细胞衰老。我们进一步通过转录组测序、生物信息学分析以及验证实验发现CircSLC39A8起到miRNA海绵（miRNA sponge）的作用，进而解除miR-23a-3p对DUSP5的抑制，提高DUSP5的表达，并通过抑制ERK活化发挥抗衰老作用，从而延缓OA进程。本项目拟在此基础上，在体内体外水平研究CircSLC39A8/miR-23a-3p/DUSP5信号轴对OA的作用及调控机制。为以该信号轴为靶点治疗OA提供实验依据和方法借鉴，以期为OA的防治提供一种新方法和新思路。

Chondrocyte senescence is the important pathogenic mechanisms of OA. Animal experiments have shown that inhibiting chondrocyte senescence can delay OA, but the specific regulatory mechanism is still unclear. In our previous study, CircSLC39A8 expression was significantly decreased in OA tissue by high-throughput sequencing, and silence CircSLC39A8 could induce chondrocyte senescence. Further big data and bioinformatics database analysis revealed that CircSLC39A8 may regulate miR-23a-3p as ceRNA, and then regulate DUSP5, thereby alleviating the OA process by Inhibiting the ERK pathway. On this basis, this study aims to investigate the effect and regulatory mechanism of CircSLC39A8/miR-23a-3p/ DUSP5 signaling axis on OA in vitro and in vivo. To provide experimental basis and method reference for the treatment of osteoarthritis, in order to provide a new method and new idea for the prevention and treatment of OA.