摘要INTRODUCTIONOsteoarthritis (OA) is a chronic low-degree inflammatory disease mainly characterized by progressive degeneration of articular cartilage, thickening of the subchondral bone, synovial inflamma-tion, meniscus and ligament degeneration, and osteophyte forma-tion.1–2 The well-established risk factors for OA include age, sex, obesity, trauma, metabolism, and joint biomechanics.3–5 The chronic pain and dysfunction caused by OA affect over 250 million people worldwide,2 which severely reduces the life quality of individuals and represents a considerable socioeconomic burden.6 Currently, drug therapy serves as a fundamental strategy in the overall treatment of OA.7–8 Throughout the whole treatment process, most patients need short-term or long-term medication,7–9 including nonsteroidal anti-inflammatory drugs (NSAIDs), opioids, and drugs for intra-articular injection (e.g., hyaluronic acid and glucocorticoid). However, the current drug treatment of OA suggested by international guidelines is merely aimed at remission of disease symptoms, without substantial interruption of the destructive process or restoration of lesioned cartilage in OA.8–10 As for patients with end-stage OA, joint arthroplasty surgery represents a prevalent treatment modality, although sometimes the functional outcome can be unsatisfactory. Moreover, joint replacement requires more revision surgery in the case of complications such as infection and prosthetic fracture.11–12 Therefore, it is essential to clarify the molecular mechanisms underlying OA occurrence and progression to facilitate new therapies for future clinical needs.