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Updated: Jun 11, 2025
Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
Transcriptomic Analysis of Cardiac Tissues in a Rodent Model of Coronary Microembolization
Zhaochang Jiang1, Haohao Lu2, Beibei Gao3
1Department of Pathology, Second Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou, Zhejiang, 310009, People's Republic of China.
Purpose:
Coronary microembolization (CME) can result in cardiac dysfunction, severe arrhythmias, and a reduced coronary flow reserve. Impairment of mitochondrial energy metabolism has been implicated in the progression and pathogenesis of CME; however, its role remains largely undetermined. This study aimed to explore alterations in mitochondria-related genes in CME.
Methods:
A rat model of CME was successfully established by injecting plastic microspheres into the left ventricle. The cardiac tissues of the two groups were sequenced and mitochondrial functions were assessed.
Results:
Using RNA-Seq, together with GO and KEGG enrichment analyses, we identified 3822 differentially expressed genes (DEGs) in CME rats compared to control rats, and 101 DEGs were mitochondria-related genes. Notably, 36 DEGs were up-regulated and 65 DEGs were down-regulated (CME vs control). In particular, the oxidative phosphorylation (OXPHOS) and mitochondrial electron transport were obviously down-regulated in the CME group. Functional analysis revealed that CME mice exhibited marked reductions in ATP and mitochondrial membrane potential (MMP), by contrast, the production of reactive oxygen species (ROS) was much higher in CME mice than in controls. Protein-protein interaction (PPI) and quantitative PCR (qPCR) validation suggested that eight hub genes including Cmpk2, Isg15, Acsl1, Etfb, Ndufa8, Adhfe1, Gabarapl1 and Acot13 were down-regulated in CME, whereas Aldh18a1 and Hspa5 were up-regulated.
Conclusion:
Our findings suggest that dysfunctions in mitochondrial activity and metabolism are important mechanisms for CME, and mitochondria-related DEGs may be potential therapeutic targets for CME.
Insights
Coronary microembolization impairs cardiac function by disrupting mitochondrial energy metabolism. This study identified key mitochondria-related genes altered in coronary microembolization, offering potential therapeutic targets.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Medicine
- Molecular Cardiology
Background:
- Coronary microembolization (CME) leads to cardiac dysfunction and arrhythmias.
- Mitochondrial energy metabolism is implicated in CME pathogenesis, but its role is not fully understood.
Purpose of the Study:
- To investigate alterations in mitochondria-related genes in a rat model of CME.
- To explore the impact of CME on mitochondrial function and gene expression.
Main Methods:
- Established a rat model of CME by injecting plastic microspheres.
- Utilized RNA-sequencing (RNA-Seq) for gene expression analysis.
- Performed Gene Ontology (GO) and KEGG pathway analyses.
Main Results:
- Identified 3822 differentially expressed genes (DEGs), with 101 being mitochondria-related.
- Observed down-regulation of oxidative phosphorylation (OXPHOS) and mitochondrial electron transport.
- Found reduced ATP and mitochondrial membrane potential (MMP), with increased reactive oxygen species (ROS) production in CME rats.
Conclusions:
- Mitochondrial dysfunction and metabolic alterations are key mechanisms in CME.
- Mitochondria-related DEGs represent potential therapeutic targets for CME treatment.
