Moreover, treatment with Fer-1 reverses the aforementioned molecular features of ferroptosis, reduces cardiac fibrosis and hypertrophy, and mitigates mitochondrial damage in cardiomyocytes, which shows similar results obtained by overexpressing SLC7A11.37 These findings indicate that the loss of ferritin in cardiomyocytes leads to heart injury and increases susceptibility to iron overload-related ferroptosis and cardiomyopathy. This evidence concerns the gene SLC7A11 and cardiomyopathy.