Key result
Integrated bioinformatics analysis identified AQP9, IL1B, and IL1RN as potential immune-related genetic biomarkers for acute myocardial infarction, with IL1RN demonstrating an AUC of 0.791.
Why the study?
Acute lesions are a leading cause of vascular-related death worldwide, but accurate genetic markers for acute myocardial infarction are lacking.
Answers are grounded in this paper and cite their sources.
Bioinformatics analysis identified AQP9, IL1B, and IL1RN as potential genetic markers and specific RNA regulatory pathways for the early diagnosis and treatment of acute myocardial infarction.
BACKGROUND: Acute lesions are among the most important causes of death due to vascular lesions worldwide. However, there are no accurate genetic markers for Acute myocardial infarction (AMI). This project will use microarray integration analysis in bioinformatics analysis to find and validate relevant AMI gene markers. METHODS: Five microarray gene expression datasets were downloaded through the GEO database. We identified 50 significant DEGs by comparing and analyzing gene expression between 92 AMI and 57 standard samples. The BioGPS database screened differentially expressed genes specific to the immune system. DEGs were mainly involved in immune-related biological processes based on Enrichment analysis. Eight hub genes and three-gene cluster modules were subsequently screened using Cytoscape and validated using Box plot's grouping comparison and ROC curves. Combined group comparison results and ROC curves analysis concluded that AQP9, IL1B, and IL1RN might be potential gene markers for the AMI process. We used the StarBase database to predict target miRNAs for eight essential genes. The expected results were used to screen and obtain target lncRNAs. Then Cytoscape was used to create CeRNA networks. By searching the literature in PubMed, we concluded that AQP9, IL1B, and IL1RN could be used as gene markers for AMI, while FSTL3-miR3303p-IL1B/IL1RN and ACSL4-miR5905p-IL1B could be used as RNA regulatory pathways affecting AMI disease progression. CONCLUSIONS: Our study identified three genes that may be potential genetic markers for AMI's early diagnosis and treatment. In addition, we suggest that FSTL3-miR-330-3p-IL1B/IL1RN and ACSL4-miR-590-5p-IL1B may be possible RNA regulatory pathways to control AMI disease progression.
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Guangyao Shao (2022) studied Acute myocardial infarction (n=201). Gene expression profiling (AQP9, IL1B, IL1RN) vs. Normal samples was evaluated on Diagnostic value (Area Under the Curve) of hub genes for acute myocardial infarction (AUC 0.791 for IL1RN, p=<0.05). Integrated bioinformatics analysis identified AQP9, IL1B, and IL1RN as potential immune-related genetic biomarkers for acute myocardial infarction, with IL1RN demonstrating an AUC of 0.791.
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