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Purpose <p>The etiology and pathogenesis of pancreaticobiliary maljunction (PBM) remain unclear, thus a comprehensive investigation of cellular diversity and microenvironmental differences is pivotal to elucidate the mechanisms driving PBM.</p> Methods <p>We performed single-cell RNA sequencing on bile duct tissues from six patients, including three with PBM and three without (non-PBM). Pathway enrichment, transcription factor analysis, and cell–cell communication were analyzed to explore cellular interactions and functional states.</p> Results <p>A total of 90,996 single cells and 11 distinct cell lineages were identified, revealing significant differences in cellular composition between the two groups. PBM group was characterized by a higher proportion of endothelial cells and fibroblasts, while B and T cells were less abundant. Three subtypes of fibroblasts, antigen-presenting, inflammatory, and myofibroblastic cancer-associated fibroblasts, with the myofibroblast subtype being predominant in PBM. We found heightened activity of the WNT and TWEAK signaling pathways in PBM, as well as increased ligand–receptor interactions between fibroblasts and other cell types, including epithelial and endothelial cells.</p> Conclusion <p>Fibroblasts play a central role in driving fibrosis and tissue remodeling in PBM through specific signaling pathways. These insights provide a foundation for future therapeutic strategies aimed at modulating fibroblast activity to prevent or mitigate fibrosis in PBM.</p>

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Diversity and heterogeneity in human pancreaticobiliary maljunction revealed by single-cell RNA sequencing

  • 期刊论文

  • 发表日期：

    2025年3月21日

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  • Hui-min Mao,
  • Wan-liang Guo,
  • San-li Shi

摘要

Purpose

The etiology and pathogenesis of pancreaticobiliary maljunction (PBM) remain unclear, thus a comprehensive investigation of cellular diversity and microenvironmental differences is pivotal to elucidate the mechanisms driving PBM.

Methods

We performed single-cell RNA sequencing on bile duct tissues from six patients, including three with PBM and three without (non-PBM). Pathway enrichment, transcription factor analysis, and cell–cell communication were analyzed to explore cellular interactions and functional states.

Results

A total of 90,996 single cells and 11 distinct cell lineages were identified, revealing significant differences in cellular composition between the two groups. PBM group was characterized by a higher proportion of endothelial cells and fibroblasts, while B and T cells were less abundant. Three subtypes of fibroblasts, antigen-presenting, inflammatory, and myofibroblastic cancer-associated fibroblasts, with the myofibroblast subtype being predominant in PBM. We found heightened activity of the WNT and TWEAK signaling pathways in PBM, as well as increased ligand–receptor interactions between fibroblasts and other cell types, including epithelial and endothelial cells.

Conclusion

Fibroblasts play a central role in driving fibrosis and tissue remodeling in PBM through specific signaling pathways. These insights provide a foundation for future therapeutic strategies aimed at modulating fibroblast activity to prevent or mitigate fibrosis in PBM.