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As illustrated in Scheme 1B, once the GCMMR NPs were endocytosed by cancer cells through the RGD-mediated targeting affinity, the outer PEG was destroyed in the acidic TME, following which MNSs converted GSH into glutathione disulfide (GSSG) and released MET to alleviate the hypoxia of TME as well as interfere with energy supply by inhibiting mitochondria-mediated respiration

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This is due to a decrease in its own synthesis