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This modulation subsequently led to the downregulation of three prime repair exonuclease 2, thereby activating the cGAS-STING pathway and mitigating immunotherapy resistance

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M2 macrophages, due to their relatively weak antioxidant defenses, undergo ferroptosis first, and the subsequent release of DAMPs and TNF- further promotes M1 polarization, rendering macrophages a factor in amplifying inflammation

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