BMC Cardiovasc Disord. 2026 May 14. doi: 10.1186/s12872-026-05822-9. Online ahead of print.
ABSTRACT
BACKGROUND: Myocardial infarction (MI), one of the most severe cardiovascular diseases, is influenced by altered macrophage status and metabolic reprogramming (MR), yet the mechanisms of their crosstalk remain unclear. This study used bioinformatics to explore key genes associated with macrophages and MR function in MI.
METHODS: Single-cell and bulk transcriptomics data of MI were obtained from public databases, and MR-related genes (MRGs) were downloaded from literature. Macrophage-associated differentially expressed genes (DEGs1) were identified from the single-cell data. Candidate genes were determined by intersecting MI-related DEGs (DEGs2), DEGs1, and MRGs. Machine learning, gene expression, and receiver operating characteristic (ROC) curve analyses were used to identify key genes. Drug prediction analysis was performed. Single-cell data were further analyzed to explore the underlying biological mechanisms of MI, followed by cell communication and pseudo-temporal analyses. Finally, RT-qPCR was used to validate the mRNA expression of key genes.
RESULTS: A total of 304 DEGs1, 1,258 DEGs2, and 1,804 MRGs were intersected, identifying 6 candidate genes. The key genes (ABCG1, GNG11, and RPL24) were successfully identified. Pathways co-enriched by key genes included Huntington's disease, olfactory transduction, oxidative phosphorylation, proteasome, and spliceosome. Two drugs targeting ABCG1, APT and vitamin E, were identified. Macrophages displayed significant interactions with B/plasma cells and dendritic cells (DC) in MI samples. The expression of ABCG1 was significantly increased in MI, while GNG11 and RPL24 were decreased.
CONCLUSION: ABCG1, GNG11, and RPL24 were identified as key regulators of macrophage function and MR in MI, providing valuable insights for the development of targeted therapies.
PMID:42135635 | DOI:10.1186/s12872-026-05822-9