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In endothelial cells (ECs), copper overload disrupts mitochondrial dynamics, increases fission and ROS production, and ultimately leads to cell death [34] In cardiomyocytes, copper promotes hypertrophy and inflammation [35], disrupts fatty acid and lipid metabolism, upregulates autophagy-associated proteins and genes, and impedes calcium ion uptake by the sarcoplasmic reticulum, thereby inhibiting myocardial contractility [36]

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lactis to counter the secondary oxidative stress induced by isoleucine starvation [72]