UnTWISTing intestinal fibrosis: single-cell transcriptomics deciphers fibroblast heterogeneity, uncovers molecular pathways, and identifies therapeutic targets

Intestinal fibrosis is a severe complication of Crohn's disease, often requiring surgical intervention. Despite extensive research efforts, an effective treatment to prevent or reverse intestinal fibrosis remains elusive. In this issue of the JCI, Zhang, Wang, and colleagues employed single-cel...

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Published inThe Journal of clinical investigation Vol. 134; no. 18; pp. 1 - 3
Main Authors Santacroce, Giovanni, Di Sabatino, Antonio
Format Journal Article
LanguageEnglish
Published United States American Society for Clinical Investigation 17.09.2024
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ISSN1558-8238
0021-9738
1558-8238
DOI10.1172/JCI184112

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Abstract Intestinal fibrosis is a severe complication of Crohn's disease, often requiring surgical intervention. Despite extensive research efforts, an effective treatment to prevent or reverse intestinal fibrosis remains elusive. In this issue of the JCI, Zhang, Wang, and colleagues employed single-cell RNA sequencing to uncover mechanisms of the fibrotic process. They identified a key fibroblast subset of TWIST1+FAP+ cells that interacts with CXCL9+ macrophages. TWIST1 emerged as a central regulator of the fibrotic microenvironment, representing a promising therapeutic target for effectively treating intestinal fibrosis.
AbstractList Intestinal fibrosis is a severe complication of Crohn’s disease, often requiring surgical intervention. Despite extensive research efforts, an effective treatment to prevent or reverse intestinal fibrosis remains elusive. In this issue of the JCI, Zhang, Wang, and colleagues employed single-cell RNA sequencing to uncover mechanisms of the fibrotic process. They identified a key fibroblast subset of TWIST1+FAP+ cells that interacts with CXCL9+ macrophages. TWIST1 emerged as a central regulator of the fibrotic microenvironment, representing a promising therapeutic target for effectively treating intestinal fibrosis.
Intestinal fibrosis is a severe complication of Crohn's disease, often requiring surgical intervention. Despite extensive research efforts, an effective treatment to prevent or reverse intestinal fibrosis remains elusive. In this issue of the JCI, Zhang, Wang, and colleagues employed single-cell RNA sequencing to uncover mechanisms of the fibrotic process. They identified a key fibroblast subset of TWISTV[FAP.sup.+] cells that interacts with [CXCL9.sup.+] macrophages. TWIST1 emerged as a central regulator of the fibrotic microenvironment, representing a promising therapeutic target for effectively treating intestinal fibrosis.
Intestinal fibrosis is a severe complication of Crohn’s disease, often requiring surgical intervention. Despite extensive research efforts, an effective treatment to prevent or reverse intestinal fibrosis remains elusive. In this issue of the JCI , Zhang, Wang, and colleagues employed single-cell RNA sequencing to uncover mechanisms of the fibrotic process. They identified a key fibroblast subset of TWIST1 + FAP + cells that interacts with CXCL9 + macrophages. TWIST1 emerged as a central regulator of the fibrotic microenvironment, representing a promising therapeutic target for effectively treating intestinal fibrosis.
Intestinal fibrosis is a severe complication of Crohn's disease, often requiring surgical intervention. Despite extensive research efforts, an effective treatment to prevent or reverse intestinal fibrosis remains elusive. In this issue of the JCI, Zhang, Wang, and colleagues employed single-cell RNA sequencing to uncover mechanisms of the fibrotic process. They identified a key fibroblast subset of TWIST1+FAP+ cells that interacts with CXCL9+ macrophages. TWIST1 emerged as a central regulator of the fibrotic microenvironment, representing a promising therapeutic target for effectively treating intestinal fibrosis.Intestinal fibrosis is a severe complication of Crohn's disease, often requiring surgical intervention. Despite extensive research efforts, an effective treatment to prevent or reverse intestinal fibrosis remains elusive. In this issue of the JCI, Zhang, Wang, and colleagues employed single-cell RNA sequencing to uncover mechanisms of the fibrotic process. They identified a key fibroblast subset of TWIST1+FAP+ cells that interacts with CXCL9+ macrophages. TWIST1 emerged as a central regulator of the fibrotic microenvironment, representing a promising therapeutic target for effectively treating intestinal fibrosis.
Audience Academic
Author Di Sabatino, Antonio
Santacroce, Giovanni
AuthorAffiliation 1 Department of Internal Medicine and Medical Therapeutics, University of Pavia, Pavia, Italy
2 First Department of Internal Medicine, San Matteo Hospital Foundation, Pavia, Italy
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CitedBy_id crossref_primary_10_1093_ibd_izaf021
crossref_primary_10_1016_j_heliyon_2024_e40604
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Copyright American Society for Clinical Investigation Sep 2024
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Snippet Intestinal fibrosis is a severe complication of Crohn's disease, often requiring surgical intervention. Despite extensive research efforts, an effective...
Intestinal fibrosis is a severe complication of Crohn’s disease, often requiring surgical intervention. Despite extensive research efforts, an effective...
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SubjectTerms Animals
Care and treatment
Cells
Colorectal diseases
Crohn Disease - genetics
Crohn Disease - metabolism
Crohn Disease - pathology
Crohn's disease
Extracellular matrix
Fibroblasts
Fibroblasts - metabolism
Fibroblasts - pathology
Fibrosis
Gastrointestinal diseases
Genetic aspects
Health aspects
Humans
Hyperplasia
Inflammation
Inflammatory bowel disease
Intestine
Intestines - pathology
Macrophages
Macrophages - metabolism
Macrophages - pathology
Medical research
Medicine, Experimental
Microenvironments
Nuclear Proteins
Pathogenesis
Physiological aspects
RNA sequencing
Single-Cell Analysis
Smooth muscle
Therapeutic targets
Transcription factors
Transcriptome
Transcriptomics
Transforming growth factors
Twist-Related Protein 1 - genetics
Twist-Related Protein 1 - metabolism
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Title UnTWISTing intestinal fibrosis: single-cell transcriptomics deciphers fibroblast heterogeneity, uncovers molecular pathways, and identifies therapeutic targets
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