ArticleFrontiers in immunology2025
Single-cell and bulk transcriptomic analyses reveal PANoptosis-associated immune dysregulation of fibroblasts in periodontitis.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Epigenetic memory in periodontal healing: mechanisms, evidence, and emerging therapeutic perspectives.Odontology · 2026Review
- Mitochondrial Calcium Overload Drives mtDNA-cGAS-STING Activation via VDAC1 and MCU Upregulation in Periodontitis.International journal of molecular sciences · 2026Article
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Authors and funding
12 authors.
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Abstract
Background: PANoptosis is a newly recognized form of programmed inflammatory cell death implicated in numerous inflammation-related diseases. However, its precise role and underlying mechanisms in periodontitis (PD) remain unclear. Methods: We analyzed single-cell RNA sequencing (scRNA-seq) on gingival tissues from PD patients and healthy individuals to profile cellular composition and quantify cell-type distributions. Functional enrichment analyses were used to explore PANoptosis and related pathways, with five gene set scoring methods applied to quantify PANoptosis activity in human gingival fibroblasts (HGFs). The expression of PANoptosis-related markers was validated by immunofluorescence staining and qPCR in HGFs and gingival tissues from PD model mice. Based on PANoptosis scores, HGFs were stratified into high- and low-activity groups. Cell-cell communication and spatial transcriptomic analyses were integrated to examine their interactions with immune cells in the periodontal microenvironment. Finally, bulk RNA-seq data were subjected to comprehensive analysis using 113 machine learning models to screen for core PANoptosis-associated genes, which were subsequently validated through qPCR and immunohistochemistry in gingival tissues. Results: scRNA-seq analysis revealed a decreased proportion of HGFs alongside enrichment of multiple PANoptosis-related pathways in PD samples. Further assessment demonstrated significantly elevated PANoptosis activity in HGFs from PD compared to controls, which was validated by tissue-level immunofluorescence staining. Conclusion: Our findings demonstrate that PANoptosis is activated in HGFs in the context of PD, which may drive immune dysregulation and facilitate disease progression. By integrating bulk transcriptomic data with machine learning algorithms, we identified and validated key PANoptosis-related genes, highlighting their potential as novel therapeutic targets.
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