<p>Myocardial infarction and gut microbiota variations are interconnected conditions that can significantly impact a patient's quality of life. Myocardial infarction, colloquially known as heart attack is&#xa0;caused by decreased or complete cessation of blood flow to a portion of the myocardium. Alterations in the gut microbiota can lead to increased inflammation, a known risk factor for myocardial infarction. The gut microbiota also produces endotoxins, which can enter the bloodstream and contribute to the development of myocardial infarction. The interplay between myocardial infarction and gut microbiota variations should be explored, emphasizing their potential as a biomarkers and potential drug targets. The current study aimed to identify, investigate and analyze the interplay and biomarkers between myocardial infarction and the gut microbiota via transcriptomics data and integrated bioinformatics analysis. Common upregulated genes were identified via R language, gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) for functional gene enrichment, and protein–protein interactions were constructed via the STRING Cytoscape plugin. Hub genes, essential modules, and drug interaction networks were identified. A total of 33 commonly upregulated genes were identified and, eight hub genes, including TLR4, TLR2, STAT3, CXCR2, CXCR4, IL1RN, CXCR1 and FCGR2A were identified. Additionally, 42 transcription factors and 23 miRNAs associated with the hub genes were identified. Furthermore, acetylcysteine, digoxin, celecoxib and osimertinib are potential drugs that interact with hub genes and are associated with the treatment of cardiovascular diseases. TLR4, TLR2, STAT3, CXCR2, CXCR4, IL1RN, CXCR1 and FCGR2A may play essential roles in myocardial infarction and gut microbiota. The predicted miRNA hsa-mir-1-3p could regulate gene expression in myocardial infarction and gut microbiota. These hub genes may contribute to the pathology and progression of myocardial infarctionand the gut microbiota, providing potential diagnostic and therapeutic opportunities patients with myocardial infarction and gut microbiota.</p>

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Bioinformatics insights into the pathogenic role of alterations in the gut microbiota in myocardial infarction via transcriptomics data

  • Abdul Qadir Nawabi,
  • Xiangwei Bo,
  • Lijuan Chen

摘要

Myocardial infarction and gut microbiota variations are interconnected conditions that can significantly impact a patient's quality of life. Myocardial infarction, colloquially known as heart attack is caused by decreased or complete cessation of blood flow to a portion of the myocardium. Alterations in the gut microbiota can lead to increased inflammation, a known risk factor for myocardial infarction. The gut microbiota also produces endotoxins, which can enter the bloodstream and contribute to the development of myocardial infarction. The interplay between myocardial infarction and gut microbiota variations should be explored, emphasizing their potential as a biomarkers and potential drug targets. The current study aimed to identify, investigate and analyze the interplay and biomarkers between myocardial infarction and the gut microbiota via transcriptomics data and integrated bioinformatics analysis. Common upregulated genes were identified via R language, gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) for functional gene enrichment, and protein–protein interactions were constructed via the STRING Cytoscape plugin. Hub genes, essential modules, and drug interaction networks were identified. A total of 33 commonly upregulated genes were identified and, eight hub genes, including TLR4, TLR2, STAT3, CXCR2, CXCR4, IL1RN, CXCR1 and FCGR2A were identified. Additionally, 42 transcription factors and 23 miRNAs associated with the hub genes were identified. Furthermore, acetylcysteine, digoxin, celecoxib and osimertinib are potential drugs that interact with hub genes and are associated with the treatment of cardiovascular diseases. TLR4, TLR2, STAT3, CXCR2, CXCR4, IL1RN, CXCR1 and FCGR2A may play essential roles in myocardial infarction and gut microbiota. The predicted miRNA hsa-mir-1-3p could regulate gene expression in myocardial infarction and gut microbiota. These hub genes may contribute to the pathology and progression of myocardial infarctionand the gut microbiota, providing potential diagnostic and therapeutic opportunities patients with myocardial infarction and gut microbiota.