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Updated: Aug 22, 2026
Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease
Published on: July 3, 2018
Downregulation of circ_0001112 Enhances Myocardial Infarction Through Regulation of miR-324-5p/CDK6 Axis
Aizhen Hu1, Lina Zhang1, Xingping Men1
1Department of Cardiology, Affiliated Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, China.
Insights
This study reveals that lower levels of circ_0001112 worsen heart attack outcomes by increasing heart cell death. This occurs through a mechanism involving miR-324-5p and CDK6, impacting myocardial infarction progression.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Mechanisms of Heart Disease
Background:
- Myocardial infarction (MI) frequently leads to heart failure (HF), necessitating a deeper understanding of its pathological basis for improved prevention and treatment.
- Identifying key molecular players in MI pathogenesis is crucial for developing targeted therapeutic strategies.
Purpose of the Study:
- To investigate the role of dysregulated circular RNA (circ_0001112) in the context of myocardial infarction (MI).
- To elucidate the molecular mechanism by which circ_0001112 influences cardiomyocyte apoptosis in MI.
Main Methods:
- Establishment of a myocardial infarction (MI) model and application of hypoxia treatment to study circ_0001112 expression.
- Luciferase assay and Ago2-miRNP immunoprecipitation to determine interactions between circ_0001112, miR-324-5p, and cyclin-dependent kinase 6 (CDK6).
- Assessment of cardiomyocyte apoptosis following manipulation of circ_0001112, miR-324-5p, and CDK6 levels.
Main Results:
- Circ_0001112 was found to be significantly upregulated in the MI model and under hypoxia.
- Overexpression of circ_0001112 inhibited hypoxia-induced cardiomyocyte apoptosis.
- Circ_0001112 acts as a sponge for miR-324-5p, which in turn targets the 3'-untranslated region (3'UTR) of CDK6.
Conclusions:
- The study demonstrates that circ_0001112 plays a protective role against cardiomyocyte apoptosis in MI.
- Downregulation of circ_0001112 promotes cardiomyocyte apoptosis by sponging miR-324-5p and consequently upregulating CDK6 expression.
- These findings identify a novel circ_0001112/miR-324-5p/CDK6 pathway implicated in the pathophysiology of myocardial infarction.
Abstract:
Myocardial infarction (MI) usually results in severe heart failure (HF), and patients suffer from the repercussions of MI, elucidation of the pathological basis of MI is crucial to optimize the prevention and treatment of MI. This study investigated the role of dysregulated circ_0001112 in MI. In our study, circ_0001112 was significantly upregulated in the MI model and by hypoxia treatment. Circ_0001112 overexpression inhibited hypoxia-induced cardiomyocyte apoptosis. Luciferase assay showed that circ_0001112 sponged miR-324-5p that regulated the expression of cyclin-dependent kinase 6 (CDK6). Ago2-miRNP immunoprecipitation further confirmed that the 3'-untranslated region (3'UTR) of CDK6 was targeted by miR-324-5p. Either miR-324-5p overexpression or CDK6 knockdown prevented cardiomyocyte apoptosis induced by circ_0001112 overexpression. In conclusion, this study demonstrated that the downregulation of circ_0001112 promoted cardiomyocyte apoptosis by sponging miR-324-5p and upregulating CDK6 expression in MI.