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Weighted gene co‑expression network analysis in identification of key genes and networks for ischemic‑reperfusion
Nan Guo1, Nan Zhang1, Liqiu Yan1
1Department of Cardiology, Cangzhou Central Hospital, Hebei Medical University, Cangzhou, Hebei 061000, P.R. China.
Insights
Acute myocardial infarction triggers heart remodeling, leading to heart failure. This study identifies key genes and networks involved in this process, offering potential therapeutic targets for inhibiting heart remodeling after infarction.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Genomics
Background:
- Acute myocardial infarction causes ventricular remodeling, a key factor in dilated cardiomyopathy and heart failure.
- The precise molecular mechanisms driving myocardium remodeling post-ischemia-reperfusion (IR) require further elucidation.
Purpose of the Study:
- To identify critical genes and molecular networks involved in myocardium remodeling following ischemia-reperfusion (IR).
- To uncover potential therapeutic targets for mitigating heart remodeling after acute myocardial infarction.
Main Methods:
- Downloaded and analyzed mRNA expression data from the National Center for Biotechnology Information database for IR hearts at days 2 and 7.
- Employed weighted gene co-expression network analysis, hierarchical clustering, protein-protein interaction (PPI) network analysis, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.
- Identified hub genes within significant modules using PPI network construction.
Main Results:
- Identified 3,321 differentially expressed genes during the heart remodeling process.
- Discovered 6 distinct modules via gene co-expression network analysis, each associated with specific biological functions and pathways.
- Highlighted key dysregulated genes, including SRC proto-oncogene, non-receptor tyrosine kinase, discs large MAGUK scaffold protein 1, ATP citrate lyase, RAN, member RAS oncogene family, tumor protein p53, and polo like kinase 2.
Conclusions:
- Heart remodeling post-IR is a complex process involving extracellular matrix organization, neural development, apoptosis, and energy metabolism.
- The identified dysregulated genes represent potential therapeutic targets for inhibiting heart remodeling following acute myocardial infarction.
Abstract:
Acute myocardial infarction induces ventricular remodeling, which is implicated in dilated heart and heart failure. The pathogenical mechanism of myocardium remodeling remains to be elucidated. The aim of the present study was to identify key genes and networks for myocardium remodeling following ischemia‑reperfusion (IR). First, the mRNA expression data from the National Center for Biotechnology Information database were downloaded to identify differences in mRNA expression of the IR heart at days 2 and 7. Then, weighted gene co‑expression network analysis, hierarchical clustering, protein‑protein interaction (PPI) network, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway were used to identify key genes and networks for the heart remodeling process following IR. A total of 3,321 differentially expressed genes were identified during the heart remodeling process. A total of 6 modules were identified through gene co‑expression network analysis. GO and KEGG analysis results suggested that each module represented a different biological function and was associated with different pathways. Finally, hub genes of each module were identified by PPI network construction. The present study revealed that heart remodeling following IR is a complicated process, involving extracellular matrix organization, neural development, apoptosis and energy metabolism. The dysregulated genes, including SRC proto‑oncogene, non‑receptor tyrosine kinase, discs large MAGUK scaffold protein 1, ATP citrate lyase, RAN, member RAS oncogene family, tumor protein p53, and polo like kinase 2, may be essential for heart remodeling following IR and may be used as potential targets for the inhibition of heart remodeling following acute myocardial infarction.
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