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Updated: Oct 26, 2025
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
miR-451 on Myocardial Ischemia-Reperfusion in Rats by Regulating AMPK Signaling Pathway
Yulin Guo1, Jie Gao1, Yan Liu1
1Department of Cardiac Surgery, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
Insights
Reducing microRNA-451 (mir-451) levels protects against myocardial ischemia-reperfusion injury by enhancing AMP-activated protein kinase (AMPK) signaling. This finding offers a potential therapeutic target for heart attack treatment.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Cellular Signaling
Background:
- Myocardial infarction (MI) is a leading cause of death in coronary heart disease patients.
- Perfusion therapy is standard for cardiovascular disease, but myocardial ischemia-reperfusion (I/R) injury remains a significant clinical challenge.
- MicroRNA-451 (mir-451) has been implicated in protecting against myocardial I/R injury via AMP-activated protein kinase (AMPK) regulation.
Purpose of the Study:
- To investigate the role of mir-451 in myocardial I/R injury in a rat model.
- To elucidate the effect of mir-451 on the AMPK signaling pathway during myocardial I/R.
Main Methods:
- Established a myocardial I/R rat model by coronary artery ligation and release.
- Modulated mir-451 expression using viral vectors and antibodies.
- Assessed AMPK signaling pathway activity, myocardial infarct size, and myocardial cell apoptosis rate.
Main Results:
- A 15.7% decrease in mir-451 expression led to an 18.3% increase in AMPK activity.
- Reduced mir-451 expression significantly decreased myocardial infarct area (by 22.4%) and myocardial cell apoptosis (by 25.2%).
- Improved pathological structure of myocardial tissue was observed with decreased mir-451 levels.
Conclusions:
- Mir-451 acts as an inhibitor of the AMPK signaling pathway.
- Decreasing mir-451 expression enhances AMPK activity, which is protective against myocardial I/R injury.
- Targeting mir-451 offers a potential therapeutic strategy to mitigate ischemia-reperfusion damage in the heart.
Abstract:
Myocardial infarction is the main cause of death in patients with coronary heart disease. At present, the main method to treat cardiovascular disease is perfusion therapy. Myocardial ischemia-reperfusion will inevitably lead to reperfusion injury, which is also a major problem in the treatment of cardiovascular diseases. It has been reported that mir-451 in microRNA family participates in the protection of myocardial ischemia-reperfusion by regulating AMPK. The aim of this study was to investigate the effect of mir-451 on myocardial ischemia-reperfusion in rats by regulating AMPK signaling pathway. Sixty adult male rats were selected to establish myocardial ischemia-reperfusion animal model by ligating and loosening coronary artery. The expression level of mir-451 was regulated by injection of mir-451 virus vector and antibody, and the effect of increased or decreased mir-451 expression level on the activity of AMPK signaling pathway was detected. The myocardial infarct area and apoptosis rate of myocardial tissue were detected after 75 min ischemia-reperfusion. The results showed that when the expression level of mir-451 decreased by 15.7%, the activity index of AMPK signaling pathway was increased by 18.3%, the infarct area was reduced by 22.4%, and the apoptosis rate of myocardial cells was decreased by 25.2%. At the same time, the pathological structure of myocardial tissue was improved. Therefore, mir-451 is an inhibitor gene of AMPK signaling pathway. Reducing the expression of mir-451 can enhance the activity of AMPK signal pathway, and the increase of AMPK signal pathway activity is beneficial to reduce myocardial ischemia-reperfusion injury.
