FIGURE 1.

Overview of the pathogenesis of OA. Current research indicates that osteoarthritis is mainly associated with excessive mechanical loading, age, gender, genetics, anatomical variations, pro-inflammatory cytokines, and oxidative stress. These factors can lead to decreased chondrocyte autophagy, increased senescence and apoptosis, enhanced generation of reactive oxygen species (ROS), and expression of matrix-degrading enzymes, such as ADAMTS-4, ADAMTS-5, MMP3 and MMP13. This imbalance disrupts the balance between anabolism and catabolism in cartilage, leading to cartilage degeneration, joint inflammation, and bone remodeling, which further impedes the normal transmission of mechanical loading to chondrocytes. Dysfunctional chondrocytes contribute to impaired maintenance of cellular homeostasis under oxidative stress, establishing a vicious cycle that ultimately leads to the occurrence of OA. Figure made by Biorender.com.