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Under neuropathological conditions, mitochondrial defects often lead to electron transfer processes and reduced NADPH oxidase activity, resulting in increased reactive oxygen species production, which weakens the redox buffering capacity of the cell and may damage key enzymes involved in energy metabolism ( Disulfidptosis is associated with the equilibrium of some redox regulatory pairs, such as cystine vs

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26, 2025, to include a statement from Novo Nordisk.