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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Li, Shihuan Li, Suqin Li, Qingjie Zhou, Qiaofeng Liao, Wenli Yu, Liangzhu Ouyang, Changhan Xia, Hongli Liu, Chao Li, Mincai |
| Abstract | Background Atherosclerosis (AS) is a chronic inflammatory disease that might induce severe cardiovascular events, such as myocardial infarction and cerebral infarction. These risk factors in the pathogenesis of AS remain uncertain and further research is needed. This study aims to explore the potential molecular mechanisms of AS by bioinformatics analyses. Methods GSE100927 gene expression profiles, including 69 AS samples and 35 healthy controls, were downloaded from Gene Expression Omnibus database and indenfied for key genes and pathways in AS. Results A total of 443 differentially expressed genes (DEGs) between control and AS were identified, including 323 down-regulated genes and 120 up-regulated genes. The Gene ontology terms enriched by the up-regulated DEGs were associated with the regulation of leukocyte activation, endocytic vesicle, and cytokine binding, while the down-regulated DEGs were associated with negative regulation of cell growth, extracellular matrix, and G protein-coupled receptor binding. KEGG pathway analysis showed that the up-regulated DEGs were enriched in Osteoclast differentiation and Phagosome, while the down-regulated DEGs were enriched in vascular smooth muscle contraction and cGMP-PKG signaling pathway. Using the modular analysis of Cytoscape, we identified 3 modules mainly involved in Leishmaniasis and Osteoclast differentiation. The GSEA analysis showed the up-regulated gene sets were enriched in the ribosome, ascorbated metabolism, and propanoate metabolism. The LASSO Cox regression analysis showed the top 3 genes were TNF, CX3CR1, and COL1R1. Finally, we found these immune cells were conferred significantly higher infiltrating density in the AS group. Conclusions Our data showed the pathway of Osteoclast differentiation and Leishmaniasis was involved in the AS process and we developed a three-gene model base on the prognosis of AS. These findings clarified the gene regulatory network of AS and may provide a novel target for AS therapy. |
| Related Links | https://bmcmedgenomics.biomedcentral.com/counter/pdf/10.1186/s12920-023-01533-8.pdf |
| Ending Page | 14 |
| Page Count | 14 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 17558794 |
| DOI | 10.1186/s12920-023-01533-8 |
| Journal | BMC Medical Genomics |
| Issue Number | 1 |
| Volume Number | 16 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2023-05-13 |
| Access Restriction | Open |
| Subject Keyword | Human Genetics Microarrays Gene Expression Atherosclerosis Differentially expressed genes (DEGs) Network modules Biomarker Bioinformatics analysis |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics (clinical) Genetics |
| Journal Impact Factor | 2.1/2023 |
| 5-Year Journal Impact Factor | 2.5/2023 |
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