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This finding is particularly significant given that some trials extended to 24 weeks of continuous exposure and included individuals with obesity-related health conditions who might have higher baseline health risks
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Pre-existing mitochondrial dysfunction due to aging, diabetes, or ischemia creates a permissive environment for cuproptosis by depleting GSH and reducing SOD2 activity, thereby compromising the organelle's ability to chelate copper and neutralize mtROS [145, 146]
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