ArticleThe Journal of clinical investigation2024
Intercellular interaction between FAP+ fibroblasts and CD150+ inflammatory monocytes mediates fibrostenosis in Crohn's disease.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Multiomic characterisation of the clinical efficacy of guselkumab induction therapy in ulcerative colitis.BMJ open gastroenterology · 2026Trial
- Serum Collagen Biomarkers Are Reflective of Tissue Specific Fibroblasts Associated With Ulcerative Colitis Activity and Treatment Response to Ustekinumab.United European gastroenterology journal · 2025Trial
- Epigenetic modulation of stromal cell states underpins pathological tissue niches in Crohn's disease.Nature immunology · 2026Article
- Multi-omics reveals fibroblast subtypes with distinct roles in inflammatory bowel disease.Biology direct · 2026Article
- Article
- From inflammation to fibrosis and cancer: the emerging role of AIEC-derived metabolites in intestinal disease progression.Experimental & molecular medicine · 2026Review
- Deciphering immune and cellular reprogramming during the progression from inflammatory bowel disease to colorectal cancer using multi-omics single-cell and spatial transcriptomics.Journal of translational medicine · 2026Article
- Article
- Tissue-layer-resolved proteome landscape of Crohn's disease strictures highlights potential drivers of fibrosis progression.JCI insight · 2026Article
- Inflammatory bowel disease and extracellular matrix: when victim becomes double agent.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Fibroblast diversity within human gut-associated lymphoid tissues.The Journal of experimental medicine · 2026Article
- Tissue resident colonic macrophages persist through acute inflammation and adapt to aid tissue repair.Mucosal immunology · 2026Article
- Article
- Elucidating a Myofibroblast-dominated Fibrotic Niche in Crohn's Disease-associated Fibrostenosis Through High-resolution Spatial Transcriptomics.Cellular and molecular gastroenterology and hepatology · 2026Article
- Expanding horizons: radiolabeled FAPI in imaging of autoimmune diseases.Frontiers in immunology · 2026Review
- Spatial fibroblast niches define Crohn's fistulae.Nature · 2026Article
- Macrophage-Orchestrated Metabolic Sensing Drives IBD Pathogenesis: A Framework for Targeted Therapy.International journal of biological sciences · 2026Review
- Mechanosensitive ion channels in intestinal homeostasis and disease.eGastroenterology · 2026Review
- Intestinal subepithelial myofibroblasts in inflammatory bowel disease: fibroblast heterogeneity, fibrosis, and therapeutic targeting.Frontiers in medicine · 2026Review
- PEGylated black-phosphorus nanosheet-alginate hydrogels enable local PRRX1 delivery to drive fibroblast reprogramming in intestinal fibrosis.Journal of nanobiotechnology · 2025Article
Corrections and comments
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Authors and funding
28 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crohn's disease (CD) is marked by recurring intestinal inflammation and tissue injury, often resulting in fibrostenosis and bowel obstruction, necessitating surgical intervention with high recurrence rates. To elucidate the mechanisms underlying fibrostenosis in CD, we analyzed the transcriptome of cells isolated from the transmural ileum of patients with CD, including a trio of lesions from each patient: non-affected, inflamed, and stenotic ileum samples, and compared them with samples from patients without CD. Our computational analysis revealed that profibrotic signals from a subset of monocyte-derived cells expressing CD150 induced a disease-specific fibroblast population, resulting in chronic inflammation and tissue fibrosis. The transcription factor TWIST1 was identified as a key modulator of fibroblast activation and extracellular matrix (ECM) deposition. Genetic and pharmacological inhibition of TWIST1 prevents fibroblast activation, reducing ECM production and collagen deposition. Our findings suggest that the myeloid-stromal axis may offer a promising therapeutic target to prevent fibrostenosis in CD.
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