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Meanwhile, knowing the mechanism of GSH-responsive and -exhausting cancer treatment strategies based on metal nanomedicines is vital for selecting an optimized approach to GSH consumption and improving the efficiency of cancer therapy

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In white adipose tissue of obese, insulin-resistant and aged mammals, NNMT is dramatically upregulated and because it consumes both the universal methyl donor (SAM) and the NAD precursor (nicotinamide), its hyperactivity simultaneously depletes the cellular methylation reserve and the NAD-salvage pool [1,2]