APOE and coronary artery disorder: Consequently, intracellular Fe2+ could not be oxidized to Fe3+ and excreted from macrophages via FPN, which may be the potential mechanism of iron retention in plaques.530 Heat shock protein 27 reduces iron absorption by downregulating TFR1, thus preventing ferroptosis and ameliorating coronary artery disease.531 Fer-1 inhibits iron accumulation, lipid peroxidation, thereby alleviating atherosclerotic damage in Apolipoprotein E-/- (ApoE-/-) mice fed a high-fat diet.532 Iron chelating agents and dietary iron restriction stabilize atherosclerotic plaques and prevent endothelial damage.532