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The proposed therapeutic mechanism involves the down-regulation of c-Jun-N-terminal kinase (JNK) by inducing Gadd45-beta activity, which ultimately disrupts a mechanism of mitochondrial damage

As a result, the ETC functioning is disrupted, and ATP content becomes significantly depleted, which breaks down metabolic and ionic homeostasis and activates the degradative enzymes such as nucleases, proteases, and phospholipases [182, 188]

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