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In contrast, cuproptosis represents a separate copper-dependent pathway in which excess copper directly targets mitochondrial metabolism, inducing cell death through aggregated lipoylated proteins and iron-sulfur (Fe-S) cluster loss, independent of apoptotic signaling [3, 8]

doi: 10.1159/000371854 85 ZhangXLiuFLanXYuLWuWWuXet al