Osteoarthritis (OA) is a common joint disease that is regarded as a local inflammatory response caused by joint instability and accompanied by the progressive degeneration of articular cartilage. However, the molecular mechanisms involved in the maintenance of articular cartilage remain a subject of debate and research. This study aims to analyze the roles of long noncoding RNA (lncRNA)-CIR and autophagy in cartilages and determine their overall contribution to the degradation of extracellular matrix. Patients with OA possessed high levels of lncRNA-CIR and MMP3 and low level of COL2A1. The levels of autophagy-related proteins, including LC3B-I/II and beclin-1, increased from 12 h to 48 h. The use of si-lncRNA-CIR reversed the trend compared with that in the OA group. The negative effect of lncRNA-CIR was assessed in vivo by establishing a model of surgically induced OA. Moreover, si-lncRNA-CIR-treated joints exhibited fewer OA changes than saline-treated joints. Results were confirmed by histopathological grading of the models by using the Osteoarthritis Research Society International Scoring System and the outcomes of immunohistochemistry for LC3B-II and MMP-3. Overall, lncRNA-CIR played a negative role in the OA process by activating autophagy. (C) 2018 Elsevier Inc. All rights reserved.