Guo Jiacheng, Yang Zhenzhen, Lu Yongzheng, Du Chunyan, Cao Chang, Wang Bo, Yue Xiaoting, Zhang Zenglei, Xu Yanyan, Qin Zhen, Huang Tingting, Wang Wei, Jiang Wei, Zhang Jinying, Tang Junnan
Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Key Laboratory of Cardiac Injury and Repair of Henan Province, Zhengzhou, Henan, 450018, China.
Bioact Mater. 2021 Aug 22;10:56-67. doi: 10.1016/j.bioactmat.2021.08.019. eCollection 2022 Apr.
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. and 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）仍然是全球发病、死亡和残疾的主要原因。活性氧（ROS）的增加是AMI后心脏过度损伤的关键因素。在此，我们开发了一种具有超氧化物歧化酶（SOD）活性的固定化酶，其与基于锆的金属有机框架（ZrMOF）交联（SOD-ZrMOF），以减轻ROS引起的损伤。有证据表明SOD-ZrMOF具有优异的生物相容性。通过有效清除ROS并抑制氧化应激，SOD-ZrMOF可以保护线粒体功能，减少细胞死亡并减轻炎症。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，促进血管生成并抑制病理性心肌重塑。因此，SOD-ZrMOF作为一种有效且安全的纳米材料治疗AMI具有巨大潜力。
