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111 This excess oxidative stress can further damage synovial cells, chondrocytes, and myocytes, disrupting energy metabolism and amplifying inflammatory signaling pathways (e.g., via NF-B and MAPK)

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This specific impairment of mitochondrial energy metabolism, combined with the downregulation of key cell cycle regulators such as c-Myc and Cyclin D1, provides a direct mechanistic explanation for the observed S-phase arrest and growth inhibition