Affiliation:
1. The Affiliated Hospital of Shandong University of Traditional Chinese Medicine
Abstract
Abstract
Background
Coronary Artery Heart Disease (CHD) is a chronic inflammatory and fibroproliferative disease background on aberrant lipid metabolism, and the focus in trending research is the mechanism of unstable plaque generated by immune-related inflammation. Identifying the mechanism of plaque-related immune infiltration is crucial for mitigating the negative effects of coronary artery disease.
Methods
The Gene Expression Omnibus (GEO) database was used to download the expression data for the CHD and control samples. The Limma R program was used to find differentially expressed genes (DEGs) between CHD and control samples. The ssGESA technique was used to examine the enrichment of 28 cell types in CHD and control samples. Using weighted gene co-expression network analysis (WGCNA), it was possible to identify modules that were important to the cell types that were differentially enriched. Following the discovery of overlapping DEGs and genes by WGCNA, a protein-protein interaction (PPI) network was built to identify hub genes. In order to assess the diagnostic utility of hub genes, ROC curves were generated. Additionally, the TF-mRNA and miRNA-mRNA regulatory networks were built and visualized by Cytoscape software, and the miRNA and TF targeting of diagnostic hub genes were predicted using the web tools miRNet and NetworkAnalyst.
Results
A total of 9485 DEGs were identified in CHD database. The results of immune cell infiltration revealed that the abundance of T follicular helper cells, type 1 T helper cells, and immature dendritic cells varied significantly between samples. The extensive immunological mechanism demonstrates the pathway involved by immune related DEGs(IR-DEGs)was primarily enriched in the peroxisome-mediated immune metabolism. Among the 421 CHD-related IR-DEGs identified, PEX6, SCP2, PEX7, PECR, SRP54, and PEX10 occupy key positions in the PPI network, featuring PEX7 as the core and five others as its interconnected genes. The ROC curve revealed that, with the exception of PECR, the other five genes had diagnostic value in the progression of CHD. The constructed miRNA and TF regulatory network model suggest that PEX7 may be casCHDed with SCP2 and PEX10 via h6a-mir-124-3p and FOXL1, which imply a molecular framework for PEX-related path.
Conclusion
Our research has elucidated the diagnostic relevance of immune-related genes, indicating that PEX7, as a potential biomarker, plays a significant role in the immune metabolism-related mechanism of CHD via the peroxisome-mediated pathway.
Publisher
Research Square Platform LLC