Identification of co-expressed central genes and transcription factors in atherosclerosis-related intracranial aneurysm

Abstract

BackgroundNumerous clinical studies have shown that atherosclerosis is one of the risk factors for intracranial aneurysms. Calcifications in the intracranial aneurysm walls are frequently correlated with atherosclerosis. However, the pathogenesis of atherosclerosis-related intracranial aneurysms remains unclear. This study aims to investigate this mechanism.MethodsThe Gene Expression Omnibus (GEO) database was used to download the gene expression profiles for atherosclerosis (GSE100927) and intracranial aneurysms (GSE75436). Following the identification of the common differentially expressed genes (DEGs) of atherosclerosis and intracranial aneurysm, the network creation of protein interactions, functional annotation, the identification of hub genes, and co-expression analysis were conducted. Thereafter, we predicted the transcription factors (TF) of hub genes and verified their expressions.ResultsA total of 270 common (62 downregulated and 208 upregulated) DEGs were identified for subsequent analysis. Functional analyses highlighted the significant role of phagocytosis, cytotoxicity, and T-cell receptor signaling pathways in this disease progression. Eight hub genes were identified and verified, namely, CCR5, FCGR3A, IL10RA, ITGAX, LCP2, PTPRC, TLR2, and TYROBP. Two TFs were also predicted and verified, which were IKZF1 and SPI1.ConclusionIntracranial aneurysms are correlated with atherosclerosis. We identified several hub genes for atherosclerosis-related intracranial aneurysms and explored the underlying pathogenesis. These discoveries may provide new insights for future experiments and clinical practice.

Identification of Co-Expressed Central Genes and Transcription Factors in Acute Myocardial Infarction and Diabetic Nephropathy

“…TLR2 is a gene encoding a Toll-like receptor family of proteins, and intervention in the TLR2 signaling pathway may be bene cial in the treatment of DN (22). TLR2 activates in ammatory responses by activating the TLR2-Myd88-NF-κB pathway, also activates immune cells to promote apoptosis (23), and is associated with the severity of coronary artery disease, plaque instability, and myocardial infarction in myocardial injury (24). High expression of FCER1G in the plasma of patients with plaque rupture (25) maybe form associated with atheromatous plaque instability by unknown mechanisms.…”

“…Macrophage polarization toward the M1 phenotype increases the risk of AMI pathogenesis and rupture and also the formation of atherosclerotic plaques by taking up LDL-ICs and converting them into foam cells (47). FcγR activates and promotes phagocytosis of macrophages, induces foam cell aggregation, and promotes the development of atherosclerotic plaques (23), inducing and exacerbating AMI and DN. Neutrophil The formation of extracellular traps (NETs) in granulocytes can be triggered by various stimuli induced by contact with surface receptors (cytokine receptors, Fcγ receptors, toll-like receptors, complement receptors, etc.)…”