دورية أكاديمية

Pharmaceutical Manipulation of Mitochondrial F0F1‐ATP Synthase Enables Imaging and Protection of Myocardial Ischemia/Reperfusion Injury Through Stress‐induced Selective Enrichment.

التفاصيل البيبلوغرافية
العنوان: Pharmaceutical Manipulation of Mitochondrial F0F1‐ATP Synthase Enables Imaging and Protection of Myocardial Ischemia/Reperfusion Injury Through Stress‐induced Selective Enrichment.
المؤلفون: Chen, Zelin, Tan, Xu, Jin, Taotao, Wang, Yu, Dai, Linyong, Shen, Gufang, Zhang, Can, Qu, Langfan, Long, Lei, Shen, Chongxing, Cao, Xiaohui, Wang, Jianwu, Li, Huijuan, Yue, Xiaofeng, Shi, Chunmeng
المصدر: Advanced Science; 3/6/2024, Vol. 11 Issue 9, p1-15, 15p
مصطلحات موضوعية: REPERFUSION, MYOCARDIAL ischemia, REPERFUSION injury, MITOCHONDRIA, MEMBRANE potential, MITOCHONDRIAL membranes, CALCIUM channels
مستخلص: To rescue ischemic myocardium from progressing to myocardial infarction, timely identification of the infarct size and reperfusion is crucial. However, fast and accurate identification, as well as the targeted protection of injured cardiomyocytes following ischemia/reperfusion (I/R) injury, remain significantly challenging. Here, a near infrared heptamethine dye IR‐780 is shown that has the potential to quickly monitor the area at risk following I/R injury by selectively entering the cardiomyocytes of the at‐risk heart tissues. Preconditioning with IR‐780 or timely IR‐780 administration before reperfusion significantly protects the heart from ischemia and oxidative stress‐induced cell death, myocardial remodeling, and heart failure in both rat and pig models. Furthermore, IR‐780 can directly bind to F0F1‐ATP synthase of cardiomyocytes, rapidly decrease the mitochondrial membrane potential, and subsequently slow down the mitochondrial energy metabolism, which induces the mitochondria into a "quiescent state" and results in mitochondrial permeability transition pore inhibition by preventing mitochondrial calcium overload. Collectively, the findings show the feasibility of IR‐780‐based imaging and protection strategy for I/R injury in a preclinical context and indicate that moderate mitochondrial function depression is a mode of action that can be targeted in the development of cardioprotective reagents. [ABSTRACT FROM AUTHOR]
Copyright of Advanced Science is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
قاعدة البيانات: Complementary Index
الوصف
تدمد:21983844
DOI:10.1002/advs.202307880