Abstract
Background: Pulpitis, a common inflammation of the dental pulp, involves intricate mechanisms that are not yet fully understood. Our study aims to elucidate the alterations in genetic transcription linked to glycolysis in pulpitis and their impact on biological pathways and molecular networks.
Methods: Gene expression data was collected from the GEO database. Glycolysis-related genes were identified through databases like GeneCards and MsigDB. To understand the roles of these genes, GO, KEGG pathway enrichment, and GSEA were carried out. The PPI network was constructed with STRING, and central genes were determined using cytoHubba algorithms. mRNA-miRNA and mRNA-TF regulatory interactions were obtained from TarBase, ChIPBase, and hTFtarget. We assessed differential expression of the hub genes between groups, and conducted ROC curve analysis. ssGSEA was used to examine immune cell infiltration, with pheatmap illustrating associations between hub genes and immune cells. All statistical analyses were performed using R.
Results: Our analysis revealed 3480 differentially expressed genes (DEGs) in pulpitis, comprising 1591 upregulated and 1889 downregulated genes. Among these, 63 glycolysis-related differentially expressed genes (GRDEGs) were predominantly located on chromosome 11. These GRDEGs were enriched in energy metabolism processes, organelle compartments, and molecular functions, implicating key pathways in the pathology of pulpitis. PPI network analysis identified eight hub genes—HIF1A, LDHA, HK2, STAT3, TALDO1,PPARG, ALDOC, and PFKP. Additionally, ssGSEA uncovered notable differences in the infiltration levels of 28 types of immune cells between pulpitis and control samples, suggesting alterations in the immune response related to pulpitis.
Conclusion: Our research offers new perspectives into the molecular mechanisms of pulpitis, particularly regarding glycolytic pathways. These results may help identify better diagnostic markers and therapeutic targets for managing pulpitis. Future studies should aim to validate these potential biomarkers and investigate their functional roles in the etiology of disease.