Differential expression of glycolysis-related genes and their potential immune mechanisms in acute myocardial infarction.

BACKGROUND: Acute myocardial infarction (AMI) remains a leading cause of global morbidity and mortality, necessitating deeper insights into its molecular mechanisms. Glycolysis, the metabolic pathway that converts glucose into pyruvate, plays a crucial role in cardiovascular diseases. This study aimed to identify glycolysis-related genes associated with AMI through integrative bioinformatics analyses.

METHODS: Gene expression profiles from GSE48060 and GSE29532 datasets were merged and analyzed to identify differentially expressed genes (DEGs) related to glycolysis in AMI. Functional enrichment, protein-protein interaction, and immune infiltration analyses were performed using various bioinformatics tools.

RESULTS: Eleven glycolysis-related DEGs were identified, with PYGL, HK3, PGAM2, PFKFB3, and PRKACB emerging as hub genes, which were further verified by quantitative real-time PCR. These genes were enriched in pathways related to muscle contraction, hexose metabolism, and fructose/mannose metabolism. Immune infiltration analysis revealed significant differences in several immune cell populations between AMI and control samples.

CONCLUSIONS: Our findings provide new perspectives on the molecular underpinnings of AMI, highlighting potential therapeutic targets and biomarkers for further investigation. Further experimental validation is necessary to confirm the functional roles of these genes in the pathogenesis of AMI.