Table 1.

Treatment strategy of ferroptosis in cardiovascular diseases.

Reagents	Key mechanisms	Protective effects	References
Fer-1 DXZ	Prevent lipid peroxidation	Maintain the function of mitochondrial, reduce endoplasmic reticulum stress, and prevent DOX-induced cardiomyopathy.	18
MitoTEMPO	Scavenge lipid peroxidation specifically in the mitochondria	Attenuate DOX-induced cardiomyopathy	18
Lip-1	Increase GPX4 protein levels and reduce ROS generation	Reduce myocardial infarct size and ischemia/reperfusion injury	51
mTOR	Regulate cellular iron transport and reduce ROS production	Protect cardiomyocytes against excess iron and ferroptosis	53
Puerarin	Regulate the expression of NOX4 and GPX4	Restore cell viability and prevent heart failure induced by pressure overload.	57
ENPP2	Reduce ROS generation caused by erastin	Protect cardiomyocytes from erastin-induced ferroptosis	58

DOX, doxorubicin; DXZ, dexrazoxane; Fer-1, ferrostatin-1; GPX4, glutathione peroxidase 4; Lip-1, liproxstatin-1; mTOR, mechanistic target of rapamycin; NOX4, NADPH oxidase 4; ROS, reactive oxygen species.