What question did this study set out to answer?

This research aims to explore the involvement of metal ion transport-related genes in the pathology of myocardial infarction through transcriptomic analysis.

April 12, 2026Open Access

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

Key Result

Ace, Igf1, Lgals3, and Serpine1 are key metal ion transport-related hub genes in myocardial infarction that positively correlate with macrophage and monocyte infiltration.

Key Points

This research aims to explore the involvement of metal ion transport-related genes in the pathology of myocardial infarction through transcriptomic analysis.
Screening of differentially expressed genes in myocardial infarction samples
Protein-protein interaction network analysis to identify hub genes
Gene set enrichment and immune infiltration analyses to understand regulatory mechanisms
Validation of expression levels for key identified genes
Molecular docking to study drug interactions with hub genes
Identified four hub genes: Ace, Igf1, Lgals3, and Serpine1 associated with metal ion transport in myocardial infarction
Increased infiltration of innate immune cells and decreased infiltration of adaptive immune cells observed in myocardial infarction
Hub genes correlated positively with macrophages and monocytes
Potential drugs predicted for the identified hub genes with strong binding capacities in molecular docking analysis

Structured PICO

Population

Transcriptome and bioinformatics data related to myocardial infarction

Outcome

Identification of hub genes and mechanisms related to metal ion transport in myocardial infarctionsurrogate

Bioinformatics analysis identified Ace, Igf1, Lgals3, and Serpine1 as key metal ion transport-related genes in myocardial infarction, offering potential new therapeutic targets.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

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.