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Nevertheless, feeding these mice a high-iron diet caused extreme cardiac injury and hypertrophic cardiomyopathy, with molecular functions typical of ferroptosis, including decreased glutathione (GSH) levels and increased lipid peroxidation. Ferrostatin-1, a specific inhibitor of ferroptosis, rescued this phenotype, supporting the idea that ferroptosis plays a pathophysiological part within the heart. Eventually, we found that Fth-deficient cardiomyocytes have paid off expression as
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