SULF1 and EPB41L3: Potential Biomarkers of Acute Myocardial Infarction and the Vascular Inflammatory Milieu

<h4>Background and objective</h4>Coronary endothelial dysfunction is considered one of the key pathological components in acute myocardial infarction (AMI). This study aimed to explore the expression patterns and potential significance of the differentially expressed genes SULF1 and EPB41L3 in AMI by integrating bioinformatics analysis and clinical validation.<h4>Methods</h4>Differentially expressed genes (DEGs) were screened from two public microarray datasets (GSE66360 and GSE132651). Their functional profiles were summarized via Gene Ontology and pathway analysis. In parallel, whole-blood samples from 29 patients with coronary artery disease were collected, and gene expression was measured using quantitative real-time PCR (qPCR). Multivariate logistic regression was adjusted, and bootstrap resampling was applied to assess robustness. Exploratory single-cell expression analysis and drug-gene interaction prediction were also performed.<h4>Results</h4>Bioinformatics analysis identified SULF1 and EPB41L3 as consistently upregulated in AMI. In clinical samples, both genes showed significantly higher expression in AMI patients compared with non-obstructive coronary artery disease controls (P=0.036 and 0.021), and this association remained significant after multivariate adjustment (P=0.039 and 0.034). Single-cell data indicated expression in endothelial cells and fibroblasts. Drug prediction suggested metoprolol and paclitaxel as potential modulators of SULF1.<h4>Conclusion</h4>This study, through integrated analysis, first validated the upregulated expression of candidate biomarkers SULF1 and EPB41L3 in the peripheral blood of AMI patients within a clinical cohort. Combined with their baseline expression profiles in cell types associated with vascular inflammation such as endothelial cells, these findings suggest that these two genes may be involved in the pathological process of AMI. This research provides new candidate targets and clues for exploring the molecular mechanisms of AMI.