Abstract

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.

Highlights

  • acute myocardial infarction (AMI) is the main cause of persistent increases in human morbidity and mortality due to obstruction of coronary blood flow [1]

  • Mice were randomly divided into 4 groups: (1) sham group, (2) AMI+PBS group (AMI mice injected with PBS via tail vein), (3) AMI+miR-383-5p agomir group (AMI mice with miR-383-5p agomir injected via tail vein), and (4) AMI+miR-383-5p agomir NC group (AMI mice with miR-383-5p agomir NC injected via tail vein)

  • phosphofructokinase muscle-type (PFKM) Can Be Predicted Involving in Regulating the Oxidative Stress

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Summary

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). 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. 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 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

Introduction
Materials and Methods
Results
Discussion
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