Related Experiment Video
Updated: Nov 5, 2025

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
miR-30c-5p acts as a therapeutic target for ameliorating myocardial ischemia-reperfusion injury
Shuping Meng1, Yanlei Hu1, Jialu Zhu1
1Cardiovascular Surgery Intensive Care Unit, Heart Center of Henan Province People's Hospital (Central China Fuwai Hospital) Zhengzhou 450003, Henan, China.
Insights
Plasma miR-30c-5p is a valuable biomarker for coronary heart disease (CHD) screening and prognosis. Lower miR-30c-5p levels indicate poor prognosis and can be targeted for therapeutic strategies in CHD.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Biomarker Discovery
Background:
- Coronary heart disease (CHD) is a leading cause of global mortality and disability.
- MicroRNAs (miRNAs) show potential as plasma biomarkers for CHD screening and prognosis.
- Understanding miRNA molecular mechanisms can reveal therapeutic targets for CHD.
Purpose of the Study:
- To investigate the role of plasma miR-30c-5p in coronary heart disease (CHD).
- To explore the correlation of miR-30c-5p with clinical characteristics and prognosis of CHD patients.
- To elucidate the molecular mechanism of miR-30c-5p in myocardial ischemia/reperfusion (I/R) injury.
Main Methods:
- Plasma samples from CHD patients and controls were analyzed for miR-30c-5p expression.
- Correlation analysis was performed between miR-30c-5p levels and clinical factors.
- Prognostic value of miR-30c-5p was assessed using receiver operating characteristic (ROC) curve analysis.
- H9C2 cell and rat myocardial I/R models were established to study miR-30c-5p and BCL2L11 interactions.
- In vitro and in vivo experiments evaluated the effects of modulating miR-30c-5p and BCL2L11 on myocardial injury.
Main Results:
- Plasma miR-30c-5p expression was significantly lower in CHD patients compared to controls.
- miR-30c-5p levels correlated with clinical characteristics including age, NYHA grade, smoking, hypertension, and hyperlipidemia.
- Lower miR-30c-5p expression predicted poor CHD prognosis with an area under the curve (AUC) of ≥0.850.
- In I/R models, miR-30c-5p was downregulated while BCL2-like 11 (BCL2L11) was upregulated.
- Upregulating miR-30c-5p or downregulating BCL2L11 improved cell proliferation and reduced apoptosis in I/R injury.
- BCL2L11 is negatively regulated by miR-30c-5p, and this interaction impacts myocardial I/R injury in vitro and in vivo.
Conclusions:
- Plasma miR-30c-5p serves as a promising diagnostic and prognostic biomarker for coronary heart disease.
- miR-30c-5p exerts protective effects against myocardial I/R injury by negatively regulating BCL2L11.
- Targeting miR-30c-5p or BCL2L11 represents a potential therapeutic strategy for CHD and related myocardial injuries.
Abstract:
Coronary heart disease (CHD) is one of the most vital reasons for death and disability all over the world. miRNA, as a plasma index, is quite valuable for disease screening and prognosis prediction in CHD. Mining the molecular mechanism behind miRNA is also helpful for us to find molecular therapeutic strategies. In this research, we found that the expression of plasma miR-30c-5p in CHD patients was obviously lower than that in the control group (CG), which had a high differential value for CHD. We also discovered that miR-30c-5p was obviously correlated with clinical characteristics of CHD patients such as age, NYHA grade, smoking history, hypertension, hyperlipidemia, etc. In prognosis analysis, the miR-30c-5p expression in patients with poor prognosis was dramatically lower than that in those with good one, and the AUC for predicting poor prognosis of CHD was not lower than 0.850. In addition, we also induced myocardial ischemia/reperfusion (I/R) injury model of H9C2 cells through hypoxia/reoxygenation, and found that H9C2 cells also had abnormally down-regulated miR-30c-5p and up-regulated BCL2-like 11 (BCL2L11). Up-regulating miR-30c-5p or down-regulating BCL2L11 were helpful to improve proliferation and apoptosis of I/R injury model. Mechanically, BCL2L11 was also negatively regulated by miR-30c-5p, and up-regulating the former could cancel the in vitro protective effect of up-regulating the latter on H9C2 cell I/R injury model. In vivo research, up-regulating miR-30c-5p or down-regulating BCL2L11 can improve myocardial injury, histopathological changes and apoptosis in rat I/R model.

