Single-Cell RNA Sequencing Reveals Pericytes Acquire a Fibrotic Phenotype and Promote Mesenteric Adipose Tissue Fibrosis in Crohn's Disease.

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Purpose Creeping fat (CF) in Crohn's disease (CD) is characterized by hyperplastic mesenteric adipose tissue (MAT) encasing fibrotic intestinal segments, marked by significant extracellular matrix (ECM) remodeling and fibrosis. Pericytes have multipotent differentiation potential, can adopt a fibrotic phenotype, and contribute to pathological ECM deposition. However, the cellular mechanisms underlying CF fibrosis remain unclear. This study aimed to elucidate the cellular origins of CF fibrosis and the involvement of pericytes. Patients and methods Histopathological analyses evaluated fibrosis in MAT samples and its correlation with adjacent muscularis propria thickening. Transcriptomic datasets and immunofluorescence confirmed fibrosis-related gene expression differences in MAT. Single-cell RNA sequencing (scRNA-seq) was analyzed to evaluate ECM production across cell types and identify pericyte-specific markers. Cell proportion analyses and in vitro experiments quantified vascular endothelial and mural cell populations. CytoTRACE and pseudotime analyses mapped pericyte differentiation trajectories. Primary human MAT pericytes were isolated and stimulated with transforming growth factor-β1 (TGF-β1) to assess fibrotic phenotype transition in vitro. Results Fibrosis was evident in uninvolved MAT from CD patients (CD-MAT) and CF, with fibrosis severity in CF correlating positively

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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