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Further, targeted metabolomics and isotope tracing experiments uncovered GGCT as a metabolic orchestrator to prioritize Gln to GSH flux for antioxidant defense, while activating glucose (Glc)-fueled anaplerosis to replenish TCA intermediates to fuel proliferation
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A deeper understanding of these interconnected metabolic networks clarifies the critical role of ferroptosis in OA progression and lays a robust foundation for integrated therapeutic strategies targeting both metabolic reprogramming and ferroptosis
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