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Kuankuan Lu, Dr

In the heart under pressure overload, intracellular copper accumulation can trigger cardiomyocyte cuproptosis via FDX1 activation, leading to lipoylated protein aggregation and mitochondrial damage, thereby exacerbating cardiac injury [12]

Given the emerging link between ferroptosis and SLE, it can be postulated that ferroptosis is an integral component in the vicious cycle of immune dysfunction, inflammation, and tissue damage in SLE pathogenesis