Key result
Nanozymes attenuate preclinical myocardial injury by targeting ferroptosis, oxidative stress, and iron homeostasis.
Why the study?
Ferroptosis has emerged as an important mechanism and potential therapeutic target in myocardial damage, and nanozymes offer a multifunctional approach to regulate oxidative stress, iron metabolism, lipid peroxidation, and inflammation.
Do nanozyme-mediated interventions regulate ferroptosis to reduce cardiomyocyte death, inflammation, and adverse remodeling in myocardial injury?
Do nanozyme-mediated interventions regulate ferroptosis to reduce cardiomyocyte death, inflammation, and adverse remodeling in myocardial injury?
This mini-review highlights the potential of multifunctional nanozymes to attenuate myocardial injury by targeting ferroptosis pathways, while outlining critical translational barriers in cardiac targeting, pharmacokinetics, and long-term biosafety.
Answers are grounded in this paper and cite their sources.
Preclinical nanozyme data support targeted ferroptosis research; leaves open clinical translation pending safety validation.
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.
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Qi et al. (2026) conducted a review in Myocardial injury (including myocardial ischemia-reperfusion injury, chemotherapy-induced cardiotoxicity, septic cardiomyopathy, and heart failure). Nanozymes (nanomedicine-mediated ferroptosis regulation) was evaluated. Nanozymes show preclinical promise in attenuating myocardial injury by modulating ferroptosis, oxidative stress, and iron homeostasis, though clinical translation requires safety validation.
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