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mitoCDN is a mitochondria-targeted copper (Cu) chelator designed to prevent mitochondrial copper overload and subsequent cuproptosis (copper-dependent cell death). In preclinical research, mitoCDN has been shown to mitigate the pro-atherogenic effects of disturbed blood flow, which induces endothelial cell dysfunction by driving copper into the mitochondria. By sequestering mitochondrial copper, mitoCDN prevents the aggregation of dihydrolipoamide S-acetyltransferase (DLAT) and the loss of Fe-S cluster proteins, thereby preserving oxidative phosphorylation and reducing endothelial cell death. In animal models, treatment with mitoCDN has demonstrated the ability to restore mitochondrial function and significantly decrease the formation of atherosclerotic lesions.
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