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Cu 2+ , which released from decomposed CCF in an acidic environment, triggered GSH exhaustion (Figure 5A) and Cu + -mediated Fenton-like reaction, avoiding the potential OH elimination

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This stress leads to suppression of forkhead box O1 (FoxO1) signaling and subsequent upregulation of thioredoxin interacting protein, inhibition of insulin and SOD-2 expression, re-expression of Neurog3, and -cell dedifferentiation and functional failure

Wang, X., S