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This review highlights the role of ferroptosis in chondrocyte malfunction and apoptosis, inflammation, and extracellular matrix breakdown, which are central to OA pathogenesis

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Transcriptomic surveys have expanded this map by detecting receptor transcripts in white and brown adipocytes, renal tubular epithelium, and activated microglia, where stimulation blunts nuclear factor kappa-B (NF-B) signaling and cytokine release, thereby linking GLP-1R to metabolic and neuro-immune regulation [31]

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