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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.
Journal of Inflammation Research
|September 30, 2024
Summary
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.
