Evidence map›Paper›PMID 40410354›Full record

ArticleScientific reports2025

Delivery of bone marrow mesenchymal stem cell-derived exosomes into fibroblasts attenuates intestinal fibrosis by weakening its transdifferentiation via the CCN2-TGF-β axis.

Fangmei Ling, Wenkai Yang, Meng Yuan, Yidong Chen, Junrong Li, Jinhua Wu, Liangru Zhu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Fangmei Ling *Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1277, Jiefang Avenue, Wuhan, 430022, Hubei province, China.
Wenkai Yang *Department of Gastroenterology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530000, China.
Meng YuanPediatric Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Yidong ChenDivision of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1277, Jiefang Avenue, Wuhan, 430022, Hubei province, China.
Junrong LiDivision of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1277, Jiefang Avenue, Wuhan, 430022, Hubei province, China.
Jinhua WuDepartment of Gastroenterology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, 530000, China.
Liangru ZhuDivision of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1277, Jiefang Avenue, Wuhan, 430022, Hubei province, China. zhuliangru@hust.edu.cn.

Funding

National Key Research and Development Program of China 2023YFC2507300National Natural Science Foundation of China 82170547Natural Science Foundation of Guangxi Zhuang Autonomous Region 2024GXNSFBA010039Natural Science Foundation of Guangxi Zhuang Autonomous Region 2024GXNSFBA010253
6 · The paper itself

Abstract

Intestinal fibrosis represents a clinically intractable complication in colitis management. This study elucidates the regulatory mechanisms by which bone mesenchymal stem cell-derived exosomes (BMSC-Exo) modulate the myofibroblastic transdifferentiation of intestinal fibroblast. BMSC-Exo was isolated and characterized. RNA sequencing was performed on TGF-β-activated CCD-18Co fibroblasts following BMSC-Exo intervention. Histopathology, immunoblotting, migration assays, and imaging techniques (immunofluorescence/immunohistochemistry) were employed to quantify extracellular matrix (ECM) deposition and fibrotic responses in both in vitro and murine models. Human colonic specimens from Crohn's disease (CD) patients with structuring complications were analyzed for fibrotic components. BMSC-Exo was successfully isolated. BMSC-Exo treatment significantly attenuated fibroblast activation and migratory capacity, concomitant with downregulating collagen I and N-cadherin expression. In vivo, histological fibrosis score, collagen deposition, and α-SMA expression were significantly decreased after BMSC-Exo administration. Transcriptomic profiling revealed significant enrichment of ECM remodeling pathways following BMSC-Exo intervention, with connective tissue growth factor (CCN2) identified as a pivotal mediator. Functional validation through CCN2 overexpression demonstrated the mechanistic dependence of BMSC-Exo's anti-fibrotic effects on the CCN2-TGF-β axis. Clinical specimens revealed a marked increase in collagen fiber deposition and co-upregulation of CCN2 in stenotic CD tissues compared to non-strictured regions. BMSC-Exo exerts potent anti-fibrotic effects through the suppression of fibroblast differentiation, mediated by targeted inhibition of the CCN2-TGF-β signaling nexus. These findings establish exosome-based therapy as a novel therapeutic strategy for intestinal fibrosis.

Indexed as

Cell TransdifferentiationConnective Tissue Growth FactorExosomesFibroblastsIntestinesMesenchymal Stem CellsTransforming Growth Factor betaAnimalsCrohn DiseaseExtracellular MatrixFibrosisHumansMaleMiceSignal TransductionCCN2 protein, humanConnective Tissue Growth FactorTransforming Growth Factor betaBone marrow mesenchymal stem cellsConnective tissue growth factorExosomesIntestinal fibrosis

Identifiers

PMID40410354
PMCPMC12102385

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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 OpenQuestion graph.