Nanomedicine-mediated ferroptosis regulation in myocardial injury: Emerging opportunities and translational challenges

Ferroptosis is a dependent and controlled form of cell death, which is characterized by lipid peroxidation and impaired antioxidant defense, and has become an important mechanism of myocardial damage. It promotes myocardial ischemia-reperfusion injury (MIRI), chemotherapy-induced cardiotoxicity, septic cardiomyopathy, and pathological remodeling, making it a potential therapeutic target. A nanozyme is a nanomaterial with enzyme mimicking catalytic activity, which provides a multifunctional method for oxidative stress regulation, iron metabolism, lipid peroxidation, and inflammation. In this mini-review, we summarize the participation of ferroptosis in myocardial lesions and its main treatment goals, as well as the recent use of nanozymes to reduce cardiac inflammation, myocardial cell death, fibrosis, and adverse remodeling. Although some studies provide direct evidence of ferroptosis regulation, the nanozyme-mediated heart protection mechanism has not been fully defined. Problems such as cardiac targeting, biosafety, pharmacokinetics, biodegradability, and clinical verification also limit translation. Subsequently, the development of nanozymes that are targeted to the heart and mechanically determined can promote clinical research on the regulation of ferroptosis during myocardial lesions.