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Hyperglycemia triggers oxidative stress in mitochondria, which significantly contributes to the development of diabetic microvascular complications [7]

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These modifications regulate various aspects of target proteins, including their activity, stability, interactions with other proteins, and intracellular localization [34]

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Its expression and activity are altered in OA cartilage under pathological conditions, suggesting a crucial role for GPX4 in OA pathogenesis and treatment