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Knockdown of circ_0060745 alleviates acute myocardial infarction by suppressing NF-κB activation
Changlin Zhai1,2, Gang Qian1,2, Huajun Wu2
1Department of Cardiovascular Diseases, The Affiliated Hospital of Jiaxing University, Zhejiang, China.
Insights
Circular RNAs (circRNAs) play a role in heart disease. This study shows circ_0060745 knockdown mitigates acute myocardial infarction (AMI) by reducing inflammation and cardiomyocyte apoptosis.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Non-coding RNA Research
Background:
- Circular RNAs (circRNAs) are increasingly recognized for their roles in cardiovascular diseases.
- The specific involvement of circRNAs in acute myocardial infarction (AMI) remains underexplored.
- Understanding novel molecular mechanisms in AMI is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role and mechanism of circ_0060745 in the pathogenesis of acute myocardial infarction (AMI).
- To determine the expression pattern and functional impact of circ_0060745 in cardiac fibroblasts and cardiomyocytes during AMI.
Main Methods:
- Expression analysis of circ_0060745 in myocardial tissue from AMI mouse models.
- In vivo knockdown of circ_0060745 to assess effects on infarct size and cardiac function.
- In vitro studies using cardiac fibroblasts to evaluate effects on macrophage migration, cardiomyocyte apoptosis, and inflammatory cytokine expression under hypoxic conditions.
- Analysis of NF-κB signaling pathway activation.
Main Results:
- Circ_0060745 expression was significantly upregulated in the myocardium of AMI mice, primarily in myocardial fibroblasts.
- Knockdown of circ_0060745 reduced myocardial infarct size and improved cardiac systolic function post-AMI.
- Inhibition of circ_0060745 in cardiac fibroblasts suppressed macrophage migration, cardiomyocyte apoptosis, and the expression of pro-inflammatory cytokines (IL-6, IL-12, IL-1β, TNF-α) and NF-κB.
- Overexpression of circ_0060745 exacerbated cardiac dysfunction and infarct size.
Conclusions:
- Circ_0060745 plays a detrimental role in the development of AMI.
- Knockdown of circ_0060745 demonstrates therapeutic potential by mitigating AMI progression.
- The protective effects of circ_0060745 inhibition are mediated through the suppression of cardiomyocyte apoptosis and inflammation, likely via the NF-κB signaling pathway.
Abstract:
It has been shown that circRNAs are involved in the development of heart diseases. However, few studies explored the role of circRNAs in acute myocardial infarction (AMI). The present study aims to investigate the role of circ_0060745 in the pathogenesis of AMI. We found that the expression of circ_0060745 was significantly increased in the myocardium of AMI mice and was mainly expressed in myocardial fibroblasts. The knockdown of circ_0060745 decreased myocardial infarct size and improved systolic cardiac functions after AMI. The knockdown of circ_0060745 in cardiac fibroblasts inhibited the migration of peritoneal macrophage, the apoptosis of cardiomyocytes and the expressions of IL-6, IL-12, IL-1β, TNF-α and NF-κB under hypoxia. Overexpression of circ_0060745 caused an increase in infarct size and worsened cardiac functions after AMI. In summary, our findings showed that knockdown of circ_0060745 mitigates AMI by suppressing cardiomyocyte apoptosis and inflammation. These protective effects could be attributed to inhibition of NF-κB activation.
