Osteoarthritis (OA) is one of the most common joint pathologies, and chondrocyte senescence plays an important role in the development and progression in OA. Previous studies found that exercise could alleviate chondrocyte senescence, however, the exact mechanisms involved have not been fully elucidated. Current researches classified chondrocyte senescence mechanisms into two categories: replicative senescence and premature senescence. In this review, we focused on the effects of exercise on telomere length, DNA damage, inflammatory factors, autophagy, antioxidant capacity of the body, as well as insulin-like growth factor 1 and macrophages, in order to identify the role of exercise in inhibiting chondrocyte senescence and to provide new targets for the clinical treatment of OA. |