Biominerallized Noble Metal-Based RuO2 Nanozymes Against Myocardial Ischemic/Reperfusion Injury

Myocardial ischemia/reperfusion (IR) injury is the leading cause of morbidity and mortality among elderly worldwide. Oxidative burst, which involves the rapid release of reactive oxygen species (ROS), is the primary mechanism of IR-mediated myocardial dysfunction and injury. Therefore, ROS elimination shows great potential for modulating IR injury. Herein, BSA-coated RuO2 nanoparticles (RuO2@BSA, RA NPs) as free radical scavengers are synthesized and their therapeutic effect against myocardial IR injury is explored. The in vitro antioxidant effect of RA NPs in cardiomyocytes is initially demonstrated. In ischemic myocardium, the RA NPs mimic multiple enzymes to remarkably reduce the infarcted area and restore cardiac function through a cascade of enzyme-like reactions, including the transformation of superoxide anion into hydrogen peroxide (H2O2) and the subsequent decomposition of H2O2 to oxygen. The therapeutic mechanism of the RA NPs is based on ROS scavenging and the inhibition of apoptosis. These findings demonstrate the high clinical potential of RA NPs in IR injury treatment.

Automated summary

Researchers have synthesized BSA-coated RuO2 nanoparticles that can scavenge reactive oxygen species and reduce myocardial ischemia/reperfusion injury. These nanoparticles mimic enzymes and can reduce infarcted areas and restore cardiac function. They have high clinical potential for IR injury treatment.