GPX4 protein levels were significantly decreased in diabetic myocardial tissues in the rabbit model, and overexpression of Nrf2 increased the expression of GPX4, which alleviated cell injury caused by high glucose.[102] Furthermore, activation of NRF2/ferroportin1 can mitigate diabetic myocardial injury by inhibiting ferroptosis.[103] Notably, the hypoglycemic agent canagliflozin has shown promise in improving DCM by suppressing ferroptosis.[104,105]. Here, NFE2L2 is linked to familial dilated cardiomyopathy.