Acute myocardial infarction (AMI) remains a dominant origin of morbidity, mortality and disability worldwide. Increases in reactive oxygen species (ROS) are key contributor to excessive cardiac injury after AMI. Here we developed an immobilized enzyme with Superoxide Dismutase (SOD) activity cross-link with Zr-based metal-organic framework (ZrMOF) (SOD-ZrMOF) for mitigate ROS-caused injury. In vitro and in vivo evidence indicates that SOD-ZrMOF exhibits excellent biocompatibility. By efficiently scavenging ROS and suppressing oxidative stress, SOD-ZrMOF can protect the function of mitochondria, reduce cell death and alleviate inflammation. More excitingly, long-term study using an animal model of AMI demonstrated that SOD-ZrMOF can reduce the infarct area, protect cardiac function, promote angiogenesis and inhibit pathological myocardial remodeling. Therefore, SOD-ZrMOF holds great potential as an efficacious and safe nanomaterial treatment for AMI.

急性心肌梗死 (AMI) 仍然是全世界发病率、死亡率和残疾的主要来源。活性氧 (ROS) 的增加是 AMI 后过度心脏损伤的关键因素。在这里，我们开发了一种具有超氧化物歧化酶 (SOD) 活性的固定化酶，与基于 Zr 的金属有机框架 (ZrMOF) (SOD-ZrMOF) 交联，以减轻 ROS 引起的损伤。体外和体内证据表明 SOD-ZrMOF 表现出优异的生物相容性。通过有效清除ROS和抑制氧化应激，SOD-ZrMOF可以保护线粒体功能，减少细胞死亡，减轻炎症。更令人兴奋的是，使用AMI动物模型的长期研究表明，SOD-ZrMOF可以减少梗死面积、保护心脏功能、促进血管生成和抑制病理性心肌重构。因此，SOD-ZrMOF 作为一种有效且安全的纳米材料治疗 AMI 具有巨大的潜力。