ArticleThe Journal of clinical investigation2024
TWIST1+FAP+ fibroblasts in the pathogenesis of intestinal fibrosis 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 46 papers.
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Who cites it
46 citing papers in PubMed.
- Serum Collagen Biomarkers Are Reflective of Tissue Specific Fibroblasts Associated With Ulcerative Colitis Activity and Treatment Response to Ustekinumab.United European gastroenterology journal · 2025Trial
- Intestinal Fibrosis in IBD: Rethinking the Inflammatory Paradigm and Emerging Therapeutic Opportunities.Digestive diseases and sciences · 2026Review
- Blocking the mCellular & molecular immunology · 2026Article
- An integrated spatially defined roadmap of normal and cancer-associated colon fibroblasts.Molecular systems biology · 2026Article
- Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.Biomarker research · 2026Review
- Review
- Epigenetic modulation of stromal cell states underpins pathological tissue niches in Crohn's disease.Nature immunology · 2026Article
- Crohn's Disease: From Immune Dysregulation to Intestinal Damage.Inflammation · 2026Review
- IL11+ fibroblasts are implicated in nonresponse to anti-TNF-α via fibrosis in inflammatory bowel disease.JCI insight · 2026Article
- Bispecific antibody engineered extracellular vesicles redirect T cells to prevent postoperative epidural fibrosis.Nature communications · 2026Article
- Multi-omics reveals fibroblast subtypes with distinct roles in inflammatory bowel disease.Biology direct · 2026Article
- Article
- Noninvasive tracking of myocardial fibrosis in pressure-overload heart failure with [EJNMMI research · 2026Article
- TNFAIP3 in M2 Macrophage Attenuates Subretinal Fibrosis in Laser-Induced Murine Model.Investigative ophthalmology & visual science · 2026Article
- Spatially Distinct Macrophage Subsets Drive Myofibroblast Heterogeneity and Maladaptive Fibrosis in Lupus Nephritis.bioRxiv : the preprint server for biology · 2026Article
- Increased remodeling of type XXII collagen is associated with an inflammatory phenotype in Crohn's disease.Scientific reports · 2026Article
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 2026Article
- Article
- Direct Extracellular Matrix Modulation Attenuates Intestinal Fibrosis via a Fibronectin-Targeted Approach.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tissue-layer-resolved proteome landscape of Crohn's disease strictures highlights potential drivers of fibrosis progression.JCI insight · 2026Article
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal fibrosis, a severe complication of Crohn's disease (CD), is characterized by excessive extracellular matrix (ECM) deposition and induces intestinal strictures, but there are no effective antifibrosis drugs available for clinical application. We performed single-cell RNA sequencing (scRNA-Seq) of fibrotic and nonfibrotic ileal tissues from patients with CD with intestinal obstruction. Analysis revealed mesenchymal stromal cells (MSCs) as the major producers of ECM and the increased infiltration of its subset FAP+ fibroblasts in fibrotic sites, which was confirmed by immunofluorescence and flow cytometry. Single-cell transcriptomic profiling of chronic dextran sulfate sodium salt murine colitis model revealed that CD81+Pi16- fibroblasts exhibited transcriptomic and functional similarities to human FAP+ fibroblasts. Consistently, FAP+ fibroblasts were identified as the key subtype with the highest level of ECM production in fibrotic intestines. Furthermore, specific knockout or pharmacological inhibition of TWIST1, which was highly expressed by FAP+ fibroblasts, could significantly ameliorate fibrosis in mice. In addition, TWIST1 expression was induced by CXCL9+ macrophages enriched in fibrotic tissues via IL-1β and TGF-β signal. These findings suggest the inhibition of TWIST1 as a promising strategy for CD fibrosis treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.