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These events lead to elevated levels of overall oxidative/antioxidant balance in vitiligo patients, which manifests as increased levels of oxidative stress and decreased antioxidant capacity, ultimately leading to vitiligo onset and lesion progression (Qiao et al., 2016)

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Both influence mitochondrial function, inflammatory tone, and the molecular machinery that governs neuronal survival and repair, engaging the same PI3K-Akt signaling pathway established earlier, now operating within neurons rather than peripheral tissue

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