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However, in OA, M2 numbers are limited and may shift toward an M1-like phenotype under sustained inflammatory stimuli, reducing their capacity to maintain iron homeostasis (109, 110).Together, these insights support the hypothesis that iron metabolism in M1 macrophages not only contributes to ferroptosis susceptibility in OA, but also represents a potential immunometabolic checkpoint for therapeutic intervention
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This delicate balance determines long-term health outcomes in ways that become increasingly clear through modern research
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