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An antioxidant nanozyme for targeted cardiac fibrosis therapy post myocardial infarction
Ziyi Gu1, Xueliang Liu1,2, Zhen Qi3
1Institute of Molecular Medicine (IMM), department of Cardiovascular Surgery, Shanghai Key Laboratory for Nucleic Acid Chemistry and Nanomedicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Abstract:
The excessive release of reactive oxygen species (ROS) after myocardial infarction (MI) disrupts the natural healing process, leading to cardiac fibrosis and compromising patient prognosis. However, the clinical application of many antioxidant drugs for MI treatment is hindered by their poor antioxidant efficacy and inability to specifically target the heart. Here we developed a tannic acid-modified MnO2 nanozyme (named MnO2@TA), which can achieve cardiac targeting to inhibit post-MI fibrosis and enhance cardiac function. Specifically, the MnO2@TA nanozyme, endowed with superoxide dismutase (SOD) and catalase (CAT) activities, effectively scavenges ROS, suppressing fibroblast activation and mitigating cardiac fibrosis without affecting cardiac repair. Notably, the incorporation of TA improves the nanozyme's affinity for the elastin and collagen-rich extracellular matrix in cardiac tissues, significantly increasing its retention and uptake within the heart and thereby enhancing its anti-fibrotic efficacy. In a murine myocardial infarction model, MnO2@TA demonstrates remarkable cardiac protection and safety, significantly improving cardiac function while attenuating cardiac fibrosis. This study presents a valuable reference for clinical research aimed at inhibiting cardiac fibrosis and advancing myocardial infarction treatments.
Insights
A novel nanozyme targets the heart to reduce scarring after heart attacks. This antioxidant therapy scavenges reactive oxygen species (ROS), inhibiting cardiac fibrosis and improving heart function in preclinical models.
Area of Science:
- Biomedical Engineering
- Nanomedicine
- Cardiovascular Research
Background:
- Myocardial infarction (MI) triggers excessive reactive oxygen species (ROS) release, impairing cardiac healing and leading to fibrosis.
- Current antioxidant therapies for MI face challenges with efficacy and cardiac targeting.
Purpose of the Study:
- To develop a cardiac-targeted nanozyme for inhibiting post-MI fibrosis and enhancing cardiac function.
- To evaluate the efficacy and safety of tannic acid-modified MnO2 nanozyme (MnO2@TA) in a murine MI model.
Main Methods:
- Development of MnO2@TA nanozyme with superoxide dismutase (SOD) and catalase (CAT) activities.
- Assessment of ROS scavenging, fibroblast activation suppression, and cardiac fibrosis mitigation.
- Evaluation of cardiac retention, uptake, and anti-fibrotic efficacy via TA modification.
- In vivo testing in a murine myocardial infarction model to assess cardiac protection and function.
Main Results:
- MnO2@TA effectively scavenges ROS, suppresses fibroblast activation, and mitigates cardiac fibrosis.
- Tannic acid (TA) modification enhances cardiac tissue retention and uptake of the nanozyme.
- In a murine MI model, MnO2@TA significantly improved cardiac function and attenuated cardiac fibrosis.
- The nanozyme demonstrated remarkable cardiac protection and safety without affecting normal cardiac repair.
Conclusions:
- MnO2@TA nanozyme offers a promising strategy for inhibiting cardiac fibrosis post-MI.
- Cardiac-targeted antioxidant nanozymes represent a valuable therapeutic approach for myocardial infarction.
- This study provides a reference for clinical research in cardiac fibrosis and MI treatment.
