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Updated: Jun 3, 2025
A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
Identification of markers correlating with mitochondrial function in myocardial infarction by bioinformatics
Wenlong Kuang1,2, Jianwu Huang3,4,5, Yulu Yang3,4,5
1Department of Cardiology, Traditional Chinese and Western Medicine Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Background:
Myocardial infarction (MI), one of the most serious cardiovascular diseases, is also affected by altered mitochondrial metabolism and immune status, but their crosstalk is poorly understood. In this paper, we use bioinformatics to explore key targets associated with mitochondrial metabolic function in MI.
Methods:
The datasets (GSE775, GSE183272 and GSE236374) were from National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO) in conjunction with mitochondrial gene data that were downloaded from the MitoCarta 3.0 database. Differentially expressed genes (DEGs) in the dataset were screened by ClusterGVis, Weighted Gene Co-Expression Network Analysis (WGCNA) and GEO2R, and functional enrichment was performed by Gene Set Enrichment Analysis (GSEA) and Kyoto Encyclopedia of Genomes (KEGG). Then mitochondria-associated DEGs (MitoDEGs) were obtained. Protein-protein interaction (PPI) networks were constructed to identify central MitoDEGs that are strongly associated with MI. The Cytoscape and miRWalk databases were then used to predict the transcription factors and target miRNAs of the central MitoDEG, respectively. Finally, the mouse model has been established to demonstrate the expression of MitoDEGs and their association with cardiac function.
Results:
MitoDEGs in MI were mainly involved in mitochondrial function and adenosine triphosphate (ATP) synthesis pathways. The 10 MI-related hub MitoDEGs were then obtained by eight different algorithms. Immunoassays showed a significant increase in monocyte macrophage and T cell infiltration. According to animal experiments, the expression trends of the four hub MitoDEGs (Aco2, Atp5a1, Ndufs3, and Ndufv1) were verified to be consistent with the bioinformatics results.
Conclusion:
Our study identified key genes (Aco2, Atp5a1, Ndufs3, and Ndufv1) associated with mitochondrial function in myocardial infarction.
