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pmid:36158806

Identification of key genes and mechanisms of epicardial adipose tissue in patients with diabetes through bioinformatic analysis.

Huiping Yang · Bingquan Xiong · Tianhua Xiong · Dinghui Wang · Wenlong Yu · Bin Liu · Qiang She

Frontiers in cardiovascular medicine · 2022 doi:10.3389/fcvm.2022.927397

Paper

complete

Experiment

complete

Data

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Analysis

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Execution

absent

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title
Identification of key genes and mechanisms of epicardial adipose tissue in patients with diabetes through bioinformatic analysis.
doi
10.3389/fcvm.2022.927397
pmid
36158806
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[0]
Huiping Yang
[1]
Bingquan Xiong
[2]
Tianhua Xiong
[3]
Dinghui Wang
[4]
Wenlong Yu
[5]
Bin Liu
[6]
Qiang She
journal
Frontiers in cardiovascular medicine
year
2022
abstract
Background: In recent years, peri-organ fat has emerged as a diagnostic and therapeutic target in metabolic diseases, including diabetes mellitus. Here, we performed a comprehensive analysis of epicardial adipose tissue (EAT) transcriptome expression differences between diabetic and non-diabetic participants and explored the possible mechanisms using various bioinformatic tools. Methods: RNA-seq datasets GSE108971 and GSE179455 for EAT between diabetic and non-diabetic patients were obtained from the public functional genomics database Gene Expression Omnibus (GEO). The differentially expressed genes (DEGs) were identified using the R package DESeq2, then Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were analyzed. Next, a PPI (protein-protein interaction) network was constructed, and hub genes were mined using STRING and Cytoscape. Additionally, CIBERSORT was used to analyze the immune cell infiltration, and key transcription factors were predicted based on ChEA3. Results: By comparing EAT samples between diabetic and non-diabetic patients, a total of 238 DEGs were identified, including 161 upregulated genes and 77 downregulated genes. A total of 10 genes (IL-1β, CD274, PDCD1, ITGAX, PRDM1, LAG3, TNFRSF18, CCL20, IL1RN, and SPP1) were selected as hub genes. GO and KEGG analysis showed that DEGs were mainly enriched in the inflammatory response and cytokine activity. Immune cell infiltration analysis indicated that macrophage M2 and T cells CD4 memory resting accounted for the largest proportion of these immune cells. CSRNP1, RELB, NFKB2, SNAI1, and FOSB were detected as potential transcription factors. Conclusion: Comprehensive bioinformatic analysis was used to compare the difference in EAT between diabetic and non-diabetic patients. Several hub genes, transcription factors, and immune cell infiltration were identified. Diabetic EAT is significantly different in the inflammatory response and cytokine activity. These findings may provide new targets for the diagnosis and treatment of diabetes, as well as reduce potential cardiovascular complications in diabetic patients through EAT modification.
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The DEGs between diabetic and non-diabetic samples were identified using the “DESeq2” package in R using an expression count profile.
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Finally, a total of 238 DEGs were identified, including 161 upregulated genes and 77 downregulated genes (Figures 2B,C).
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Finally, a total of 238 DEGs were identified, including 161 upregulated genes and 77 downregulated genes (Figures 2B,C).
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Novel Atherogenic Pathways from the Differential Transcriptiome Analysis of Diabetic Epicardial Adipose Tissue
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using various bioinformatic tools. Methods: RNA-seq datasets GSE108971 and GSE179455 for EAT bet
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Here, we performed a comprehensive analysis of epicardial adipose tissue (EAT) transcriptome expression differences between diabetic and non-diabetic participants and explored the possible mechanisms using various bioinformatic tools.\nMethods: RNA-seq datasets GSE108971 and GSE179455 for EAT between diabetic and non-diabetic patients were obtained from the public functional genomics database Gene Expression Omnibus (GEO). The differentially expressed genes (DEGs) were identified using the R package DESeq2, then Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were analyzed. Next, a PPI (protein-protein interaction) network was constructed, and hub genes were mined using STRING and Cytoscape. 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Several hub genes, transcription factors, and immune cell infiltration were identified. Diabetic EAT is significantly different in the inflammatory response and cytokine activity. 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