BACKGROUND: After osteoarthritis, chondrocyte autophagy is inhibited. Autophagy is an important physiological mechanism to maintain cell homeostasis, which reduces injury of macromolecules and organelles. Improving autophagy may alleviate the progression of osteoarthritis. OBJECTIVE: To explore the mechanism of chondrocyte autophagy in osteoarthritis and the regulation of related factors in chondrocyte autophagy. METHODS: Relevant literatures were searched in PubMed, CNKI, and WanFang from January 2001 to present, using the keywords of “osteoarthritis, chondrocyte, autophagy, treatment, signaling pathways, traditional Chinese medicine, miRNA.” RESULTS AND CONCLUSION: The progression of osteoarthritis is related to the changes of autophagy in chondrocytes. In the early stage of cartilage degeneration, autophagy in chondrocytes is activated to protect chondrocytes against various environmental changes. However, with the aggravation of cartilage degeneration, autophagy in chondrocytes cannot maintain, resulting in cell damage and even death. Protein kinases such as mammalian target of rapamycin, nuclear factor-κB, p53 and signaling pathways are involved in autophagy and its related processes. Rapamycin, diazoxide, resveratrol and microRNAs can increase the autophagy activity of chondrocytes, which is a feasible method to inhibit the progression of osteoarthritis. [ABSTRACT FROM AUTHOR]