Background Acute myocardial infarction (AMI) is a serious, deadly disease with a high incidence. However, it remains unclear how necroptosis affects the pathophysiology of AMI. Using bioinformatic analyses, this study investigated necroptosis in AMI. Methods Using the Gene Expression Omnibus (GEO) database, we obtained the GSE66360 dataset related to AMI. Venn diagrams were used to identify necroptosis-related differential genes (NRDEGs). The genes with differential expression in AMI were analyzed using gene set enrichment analysis (GSEA), and a protein-protein interaction (PPI) network was established. A transcription factor prediction and enrichment analysis was conducted for the NRDEGs, and the relationships between AMI, NRDEGs, and immune cells were determined. Finally, in the additional dataset (GSE61145), NRDEG expression levels and immune infiltration were confirmed, and gene expression levels were further verified experimentally. Results GSEA revealed that necroptosis pathways were significantly enriched in AMI. We identified 10 NRDEGs, including TNF, TLR4, FTH1 and so on. Enrichment analysis indicated that the NOD-like receptor and TNF signaling pathways were significantly enriched. Four NRDEGs, FTH1, IFNGR1, STAT3, and TLR4, were identified; however, additional datasets and further experimental validation are required to confirm their roles. In addition, we determined that a high abundance of monocytes, macrophages, neutrophils, induced Tregs, and Th2 cells prompted AMI development. Conclusions In this study, four genes with potential to affect the development of AMI through necroptosis (FTH1, IFNGR1, STAT3, and TLR4) were identified. In addition, we found that a high abundance of monocytes, macrophages, neutrophils, and Th2 cells affected AMI. This helps determine the pathological mechanism of necroptosis and immune cells that influence AMI and provides a novel strategy for targeted therapy.

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Background Increasingly, the shared risk factors and pathological processes of atherosclerosis and abdominal aortic aneurysm (AAA) are being recognized. However, the exact mechanism underlying the shared pathogenesis of atherosclerosis and AAA formation remains unclear. Methods The aim of our study was to identify the hub genes involved in the pathogenesis of atherosclerosis and AAA. Our analysis was based on two gene expression profiles for atherosclerosis (GSE28829) and AAA (GSE7084), downloaded from the Gene Expression Omnibus (GEO) database. Common differential genes were identified and an enrichment analysis of differential genes was conducted, with construction of protein-protein interaction networks, and identification of common hub genes and predicted transcription factors. Results The analysis identified 133 differentially expressed genes (116 upregulated and 17 downregulated), with the enrichment analysis identifying a potential important role of integrins and chemokines in the common immune and inflammatory responses of atherosclerosis and AAA. Regulation of the complement and coagulation cascades and regulation of the actin cytoskeleton were associated with both diseases, with 10 important hub genes identified: TYROBP, PTPRC, ITGB2, ITGAM, PLEK, CTSS, LY86, ITGAX, CCL4, and FCER1G. Conclusions Findings identified a common pathogenetic pathway between atherosclerosis and AAA, with integrin-related genes playing a significant role in both diseases. The common pathways and hub genes identified provide new insights into the shared mechanisms of these two diseases and can contribute to identifying new therapeutic targets and predicting the therapeutic effect of biological agents.