Exercise-myokine relationships in osteoarthritis

The pathogenesis and progression of osteoarthritis (OA) involve a multidimensional interplay of biomechanical abnormalities, metabolic disturbances, and inflammatory cascades. Current clinical interventions for OA face limitations such as singular therapeutic targets and significant adverse effects, highlighting an urgent need to explore innovative strategies targeting pathological network regulation.

Recent advancements have revealed that exercise training modulates OA through the "exercise-myokine-joint" regulatory axis. This axis is mediated by myokines secreted from skeletal muscle, providing a breakthrough direction for OA prevention and treatment. Studies demonstrate that physical exercise ameliorates OA progression through biomechanical adaptations, inflammatory modulation, and metabolic regulation, with myokines serving as molecular messengers that precisely regulate cartilage metabolism, inflammatory responses, and bone remodeling networks. Notably, exercise parameters (modality, intensity, frequency) exhibit dose-dependent correlations with myokine secretion profiles.

This review systematically examines the molecular basis and translational potential of the exercise-myokine-OA regulatory network, offering theoretical support for developing myokine-targeted precision interventions while pioneering novel pathways for clinical optimization of exercise therapy.