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Updated: May 5, 2026
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
CircCOL3A1 ameliorates myocardial ischemia-reperfusion injury by regulating miR-29b-3p/MDM2-mediated apoptosis
Lihua Sun1, Siyan Shi1, Weihao Wang1
1Department of Cardiology, Boai Hospital of Zhongshan, Southern Medical University, Guangdong 528405, China.
Insights
Circular RNA COL3A1 (circCOL3A1) protects against myocardial ischemia-reperfusion (I/R) injury by regulating apoptosis. This finding highlights circCOL3A1 as a potential therapeutic target for heart conditions.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Biochemistry
Background:
- Cardiovascular diseases (CVDs) are a leading global cause of death.
- Myocardial ischemia-reperfusion (I/R) injury presents a significant clinical challenge.
- Circular RNAs (circRNAs) are increasingly recognized for their roles in disease, including myocardial I/R injury.
Purpose of the Study:
- To investigate the role of circCOL3A1 in myocardial I/R injury.
- To elucidate the regulatory mechanisms involving miR-29b-3p and MDM2.
- To assess circCOL3A1 as a potential therapeutic target.
Main Methods:
- Utilized a mouse model and H9c2 cardiomyocyte cells.
- Assessed circCOL3A1 expression under I/R and hypoxia/reoxygenation (H/R) conditions via RT-qPCR.
- Employed Western blotting, TUNEL assay, and dual-luciferase reporter assays to determine molecular interactions.
Main Results:
- CircCOL3A1 expression was significantly downregulated in I/R and H/R models.
- circCOL3A1 overexpression reduced apoptosis and improved cell viability.
- These protective effects were mediated through the miR-29b-3p/MDM2 axis.
Conclusions:
- CircCOL3A1 acts as a protective factor in myocardial I/R injury.
- It functions as a miR-29b-3p sponge, regulating MDM2-mediated apoptosis.
- circCOL3A1 represents a promising therapeutic target for myocardial I/R injury.
Background:
Cardiovascular diseases (CVDs) are leading causes of mortality globally, with myocardial ischemia-reperfusion (I/R) injury being a critical challenge in clinical settings. Circular RNAs (circRNAs) have emerged as significant molecular players in various pathophysiological conditions, including myocardial I/R injury.
Objective:
This study aimed to investigate the role of circCOL3A1 in myocardial I/R injury and its potential regulatory mechanisms involving miR-29b-3p and MDM2.
Methods:
Using a mouse model and H9c2 cardiomyocyte cells, we examined the expression levels of circCOL3A1 under I/R and hypoxia/reoxygenation (H/R) conditions. We utilized RT-qPCR, Western blotting, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and dual-luciferase reporter assays to explore the interaction between circCOL3A1, miR-29b-3p, and MDM2.
Results:
CircCOL3A1 was significantly downregulated in both I/R-treated mice and H/R-treated H9c2 cells. Overexpression of circCOL3A1 reduced apoptosis and improved cell viability by modulating the miR-29b-3p/MDM2 axis. These effects were reversed by overexpressing miR-29b-3p or silencing MDM2.
Conclusions:
CircCOL3A1 plays a protective role in myocardial I/R injury by acting as a miR-29b-3p sponge, thereby regulating the MDM2-mediated apoptosis pathway. This identifies circCOL3A1 as a potential therapeutic target for treating myocardial I/R injury.
