期刊
ACS APPLIED MATERIALS & INTERFACES
卷 13, 期 45, 页码 53671-53682出版社
AMER CHEMICAL SOC
DOI: 10.1021/acsami.1c18061
关键词
myocardial ischemia/reperfusion injury; polydopamine nanoparticles; ferroptosis; reactive oxygen species; ferrous iron; cardioprotection
资金
- National Natural Science Foundation of China [81873500, 22005327]
- Applied Basic Research Program of Sichuan Science and Technology Agency [2019YJ0153]
- West China Hospital, Sichuan University [20HXBH141]
The study demonstrates that the use of PDA NPs effectively reduces Fe(2+) deposition and lipid peroxidation in a myocardial I/R injury mouse model, leading to improved cardiac function and reduced infarct size. The findings highlight the therapeutic effects of PDA NPs against myocardial I/R injury by preventing ferroptosis.
Ferroptosis is a new form of regulated cell death depending on elevated iron (Fe2+) and lipid peroxidation levels. Myocardial ischemia/reperfusion (I/R) injury has been shown to be closely associated with ferroptosis. Therefore, antiferroptosis agents are considered to be a new strategy for managing myocardial I/R injury. Here, we developed polydopamine nanoparticles (PDA NPs) as a new type of ferroptosis inhibitor for cardioprotection. The PDA NPs features intriguing properties in inhibiting Fe2+ accumulation and restoring mitochondrial functions in H9c2 cells. Subsequently, we demonstrated that administration of PDA NPs effectively reduced Fe(2+ )deposition and lipid peroxidation in a myocardial I/R injury mouse model. In addition, the myocardial I/R injury in mice was alleviated by PDA NPs treatment, as demonstrated by reduced infarct size and improved cardiac functions. The present work indicates the therapeutic effects of PDA NPs against myocardial I/R injury via preventing ferroptosis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据