Integrative transcriptomic analysis identifies ACP5 and FBLN5 as candidate shared transcriptomic signatures between pulpitis and carotid plaque rupture.

Inflammatory mediators are significant contributors to atherosclerosis and pulpitis, and the progression of atherosclerosis may result in carotid plaque rupture (CPR). The purpose of this research was to identify candidate shared transcriptomic markers between pulpitis and CPR. Transcriptome data for pulpitis and CPR were collected from the Gene Expression Omnibus (GEO) database. This study identified 629 key module genes associated with pulpitis and CPR through weighted gene co-expression network analysis (WGCNA). Among these, 13 comorbidity genes were highlighted. Functional enrichment analysis linked these genes to extracellular matrix organization and inflammatory responses (P < 0.05). Machine learning approaches prioritized ACP5 and FBLN5 as candidate transcriptomic markers, whose predictive efficacy was further validated via receiver operating characteristic (ROC) analysis, with all area under the curve (AUC) values exceeding 0.85. Furthermore, the expression levels of transcriptomic markers were validated using real-time quantitative PCR (RT-qPCR) in clinical tissues from 5 pulpitis patients and 5 independent normal controls, as well as 5 CPR patients and 5 independent control individuals. The results showed that FBLN5 was expressed at lower levels in CPR, while ACP5 was highly expressed in pulpitis (P < 0.05). Although the expression differences of ACP5 in CPR and FBLN5 in pulpitis were not statistically significant, their expression trends were basically consistent with bioinformatics results (P > 0.05). Regulatory network analysis suggested ACP5 and FBLN5 involvement in immune regulation and inflammation-driven processes. In summary, ACP5 and FBLN5 have been identified as candidate shared transcriptomic features, providing preliminary insights for future mechanistic investigations.