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Thus, the success of autophagy-targeted therapies hinges on achieving temporal and contextual specificity, activating autophagy where it is protective and inhibiting it where it is harmful

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Furthermore, phosphorylated JNK induces oxidative stress, mitochondrial membrane permeability, and dysfunction through the activation of Bax, the translocation of Bax to the mitochondria, the opening of the mitochondrial permeability transition pore, and Src-dependent inhibition of the electron transport complex