High glucose induces senescence in synovial mesenchymal stem cells through mitochondrial dysfunction

High glucose concentrations induce senescence in SMSCs via mitochondrial dysfunction, manifested as ROS accumulation, excessive fission, and mitophagy suppression. Glucose normalization reversed senescence phenotypes, accompanied by restored mitophagy and reduced oxidative stress. Mitochondrial dysfunction may be one of the key mechanisms underlying high glucose-induced senescence in SMSCs.