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Without public access to the methodology, detailed results, and pharmacokinetic data, the clinical community cannot independently scrutinize and validate the findings

This recognition step triggers further cytokine release and inflammation, thereby perpetuating an inflammationferroptosisinflammation positive feedback loop ( 4.4 Interactions between cartilage and synovium 4.4.1 Interplay between cytokines released by chondrocytes and synovial cells When cartilage is damaged, chondrocytes release proteoglycan fragments, type II collagen fragments, and diverse injury-associated factors that synovial cell surface pattern recognition receptors (PRRs) can detect, prompting synovial hyperplasia and proinflammatory cytokine secretion ( 4.4.2 Synovitis, ferroptosis, and iron homeostasis imbalance Although synovitis is not the primary lesion in OA, its role as a possible inflammatory amplifier cannot be overlooked ( During OA, synovial tissue exhibits an inflammatory response, releasing IL-1, IL-6, TNF-, and other cytokines and chemokines that attract peripheral immune cells such as macrophages, neutrophils, and T cells to the synovial membrane ( As immune cells gather and become activated in the inflamed synovium during OA, ROS production significantly increases

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