Related Experiment Video
Updated: Oct 9, 2025
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
MicroRNA-383-5p Regulates Oxidative Stress in Mice with Acute Myocardial Infarction through the AMPK Signaling
Linlin Gao1, Zhongbao Ruan1, Gecai Chen1
1Department of Cardiovascular Medicine, Taizhou People's Hospital, Taizhou, China.
Objective:
The purpose of this study is to explore the regulating role of microRNA-383-5p (miR-383-5p) in oxidative stress after acute myocardial infarction (AMI) through AMPK pathway via phosphofructokinase muscle-type (PFKM).
Methods:
We established the AMI model, and the model mice were injected with miR-383-5p agomir to study the effect of miR-383-5p in AMPK signaling pathways. The target gene for miR-383-5p was reported to be PFKM, so we hypothesized that overexpression of miR-383-5p inhibits activation of the AMPK signaling pathway.
Results:
In this research, we found that overexpression of miR-383-5p decreases myocardial oxidative stress, myocardial apoptosis, the expression level of PFKM malondialdehyde (MDA), and reactive oxygen species (ROS) in the myocardial tissues after AMI, and finally, AMI-induced cardiac systolic and diastolic function could be improved.
Conclusion:
This study demonstrated that miR-383-5p could reduce the oxidative stress after AMI through AMPK signaling pathway by targeting PFKM.
Insights
MicroRNA-383-5p (miR-383-5p) reduces oxidative stress and improves heart function after acute myocardial infarction (AMI) by targeting PFKM via the AMPK pathway.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Acute myocardial infarction (AMI) is a leading cause of heart failure.
- Oxidative stress plays a critical role in AMI pathogenesis.
- MicroRNAs are emerging as key regulators in cardiovascular diseases.
Purpose of the Study:
- To investigate the role of microRNA-383-5p (miR-383-5p) in regulating oxidative stress post-AMI.
- To elucidate the involvement of the AMPK signaling pathway and its target phosphofructokinase muscle-type (PFKM) in miR-383-5p's function.
Main Methods:
- Establishment of an AMI mouse model.
- Administration of miR-383-5p agomir to model mice.
- Analysis of AMPK signaling pathway activation and PFKM expression.
- Assessment of myocardial oxidative stress, apoptosis, and cardiac function.
Main Results:
- Overexpression of miR-383-5p significantly decreased myocardial oxidative stress markers, including malondialdehyde (MDA) and reactive oxygen species (ROS).
- miR-383-5p reduced myocardial apoptosis and suppressed PFKM expression.
- Cardiac systolic and diastolic function were improved in AMI mice treated with miR-383-5p.
Conclusions:
- miR-383-5p acts as a protective factor against oxidative stress following AMI.
- The therapeutic effect of miR-383-5p involves the AMPK signaling pathway by targeting PFKM.
- miR-383-5p represents a potential therapeutic target for managing AMI.
More Related Videos
09:53Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
05:41Left Anterior Descending Coronary Artery Ligation for Ischemia-Reperfusion Research: Model Improvement via Technical Modifications and Quality Control
Published on: December 16, 2022
