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Secondly, since cardiomyocytes are easily affected by free iron overload, the release of excess free iron during ferroptosis would result in up-regulation of transferrin receptor (TFR) and down-regulation of ferritin, promoting cardiomyocyte cell death through mitochondrial VDAC2/3 or membrane lipid peroxidation through Fenton reaction to induce myocardial edema and dysfunction (Liu et al., 2018)

Le Saux G, 2009, 'Silicon (100) electrodes resistant to oxidation in aqueous solutions: An unexpected benefit of surface acetylene moieties', Langmuir , 25, pp

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795 Therefore, FEACR and its downstream factors may be new targets for reducing ferroptosis in ischemic heart disease

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