Potential Molecular Pathway Linking Caffeine Exposure to Trigeminal Neuralgia
An In Silico Study
DOI:
https://doi.org/10.5195/d3000.2026.1605Palabras clave:
caffeine, trigeminal neuralgia, pathways, bioinformaticResumen
Trigeminal neuralgia is a debilitating neuropathic pain disorder characterized by recurrent, brief, electric shock-like facial pain. Although caffeine is widely consumed and has neuroinflammatory modulation ability, its potential molecular association with trigeminal neuralgia remains unclear. This study aimed to investigate potential molecular pathways linking caffeine exposure to trigeminal neuralgia-related biological processes. Compound-disease datasets were obtained from CTD database. Gene-gene interaction network was constructed with GeneMANIA. GO and KEGG pathway enrichment analysis were performed using DAVID bioinformatics (p-value set to 0.05; FDR-correction applied). Cell-type specific gene-expression were assessed using single-cell data from HPA server. Eight overlapping genes —FOS, GFAP, GRIN1, IL1B, MAPK1, MAPK3, MAPK9, and TNF— were recognized in caffeine-trigeminal neuralgia datasets. Gene-gene interaction network showed predominence predicted and physical interaction. Biological processes, cellular components, molecular functions, and pathway enrichment analysis were obtained. HPA analysis demonstrated gene expression across vascular and immune cell populations. Molecular overlaps, biological frameworks and pathways, showed potential trigeminal sensitization through neuroinflammation, glial response, MAPK signaling, immune-cell interaction and neural excitability. These findings provide computational evidence of potential molecular links between caffeine and mechanism underlying trigeminal neuralgia.
Citas
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