Exploration of the Potential Mechanism of Metal Ion Transport‐Related Genes in Myocardial Infarction Based on Transcriptomics

Myocardial infarction (MI), a severe coronary artery disease manifestation, is a top global cause of death. Abnormal metal ion transport (MIT) is key to MI pathological progression, and this study explores MIT's molecular characteristics/regulatory mechanisms in MI via transcriptome and bioinformatics data. Differentially expressed genes (DEGs) in MI were screened, and their intersection with MIT-related genes (MITRGs) identified candidate genes. Protein-protein interaction (PPI) network analysis, expression validation, gene set enrichment, immune infiltration analyses, and regulatory network construction were used to find hub genes and mechanisms. Through algorithmic analysis combined with gene expression validation, Ace, Igf1, Lgals3, and Serpine1 were identified as hub genes. These hub genes are mainly involved in metabolic pathways such as the TCA cycle and lysosomes. In the MI group, the infiltration of innate immune cells was increased, while that of adaptive immune cells was decreased. Additionally, Serpine1, Lgals3, Ace, and Igf1 showed a significant positive correlation with macrophages and monocytes. Various potential drugs were predicted for these hub genes. Molecular docking revealed strong binding capacities between these human hub genes and their corresponding drugs. Through bioinformatics analysis, this study identified four hub genes closely associated with MIT in MI, providing a new research basis for the mechanism of MI.