ISSN 2149-2263 | E-ISSN 2149-2271
The Anatolian Journal of Cardiology
Effects of Mitochondrial ATP-Sensitive Potassium Channel in Rats with Acute Myocardial Infarction and Its Association with the AKT/mTOR Pathway [Anatol J Cardiol]
Anatol J Cardiol. 2023; 27(2): 88-99 | DOI: 10.14744/AnatolJCardiol.2022.2406

Effects of Mitochondrial ATP-Sensitive Potassium Channel in Rats with Acute Myocardial Infarction and Its Association with the AKT/mTOR Pathway

Qian Zeng1, Long-Dan Zhang1, Quan-fang Chen2, Wei Wang1, Zhou Huang1, Dong-Ling Huang1, Fan Wang1, Feng Yang1, Jifei Nong1, Jie Yang1, Jincheng Zeng1
1Department of Emergency, the First Affiliated Hospital, Guangxi Medical University, Nanning, Guangxi, People’s Republic of China
2Institute of Respiratory Disease, the First Affiliated Hospital, Guangxi Medical University, Nanning, Guangxi, People’s Republic of China

Background: Myocardial infarction is associated with the autophagy and apoptosis of cardiomyocytes, and the protein kinase B/mammalian target of rapamycin (AKT/mTOR) pathway plays a crucial role in this mechanism.

Methods: Acute myocardial infarction rat models were assessed 0.5, 2, 4, and 6 hours after the induction of the myocardial infarction using hematoxylin and eosin staining, triphenyl tetrazolium chloride staining, myocardial enzyme measurements, and levels of autophagic activity. Additionally, diazoxide, 5-hydroxydecanoate, and LY294002 were intraperitoneally administered to rat models at peak myocardial injury to assess their effects on cardiac injury. The expression levels of autophagy-related and apoptosis-related proteins, as well as p-AKT and p-mTOR, were measured. Electron microscopy was used to assess the ultrastructure and the number of autophagosomes in the cardiac tissue.

Results: We demonstrated that the degree of myocardial injury and the level of autophagy were significantly elevated in the experimental cohort compared with the control cohort. In addition, the myocardial infarct size was significantly smaller in diazoxide-treated acute myocardial infarction rats compared with untreated rats. Diazoxide also decreased the levels of myocardial injury markers, autophagy, and apoptosis, while it also induced the levels of AKT and mTOR phosphorylation, decreased the number of autophagosomes, and improved the myocardial ultrastructure of the acute myocardial infarction rats. 5-Hydroxydecanoate treatment resulted in an opposite effect to those observed upon diazoxide treatment. LY294002 was also able to reverse diazoxide treatment effects.

Conclusion: Peak levels of myocardial tissue injury and autophagy were observed 2 hours post-acute myocardial infarction induction in rats. Diazoxide treatment inhibited myocardial autophagy and apoptosis while protecting cardiac tissue from ischemic injury, which is likely to have proceeded through activation of the AKT/mTOR pathway.

Keywords: AMI, mitochondrial ATP-sensitive potassium channel, PI3K/AKT/mTOR path-way, autophagy, apoptosis

Qian Zeng, Long-Dan Zhang, Quan-fang Chen, Wei Wang, Zhou Huang, Dong-Ling Huang, Fan Wang, Feng Yang, Jifei Nong, Jie Yang, Jincheng Zeng. Effects of Mitochondrial ATP-Sensitive Potassium Channel in Rats with Acute Myocardial Infarction and Its Association with the AKT/mTOR Pathway. Anatol J Cardiol. 2023; 27(2): 88-99

Corresponding Author: Wei Wang, China
Manuscript Language: English


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