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TP53 upregulates numerous pro-apoptotic genes including BAX, PUMA, and NOXA, promoting mitochondrial-mediated apoptosis by inducing mitochondrial outer membrane permeabilization, releasing cytochrome c, and activating downstream caspases

Treatment requires addressing both the surface pigmentation and the friction stimulus simultaneously

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Low-intensity aerobic work at this intensity preferentially burns fatty acids over glucose, which theoretically aligns with the liberated free fatty acids from AOD-9604 stimulation

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