Evidence map›Paper›PMID 37822869›Full record

ReviewFrontiers in cell and developmental biology2023

Role of the epithelial barrier in intestinal fibrosis associated with inflammatory bowel disease: relevance of the epithelial-to mesenchymal transition.

Dulce C Macias-Ceja, M Teresa Mendoza-Ballesteros, María Ortega-Albiach, M Dolores Barrachina, Dolores Ortiz-Masià

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
10.6field-weighted citation impact, top 1% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

29 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  13. Review
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  15. Article
  16. Fibrosis in Immune-Mediated and Autoimmune Disorders.Journal of clinical medicine · 2025
    Review
  17. Article
  18. The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Review
  19. Article
  20. Review
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

5 authors at 2 institutions in 1 country.

Dulce C Macias-CejaDepartamento de Farmacología and CIBEREHD, Facultad de Medicina, Universidad de Valencia, Valencia, Spain.
M Teresa Mendoza-BallesterosInstituto de Educación Superior Isabel de Villena, Conselleria de Educación, Cultura y Deporte, Valencia, Spain.
María Ortega-AlbiachINCLIVA Biomedical Research Institute, Valencia, Spain.
M Dolores BarrachinaDepartamento de Farmacología and CIBEREHD, Facultad de Medicina, Universidad de Valencia, Valencia, Spain.
Dolores Ortiz-MasiàDepartamento de Farmacología and CIBEREHD, Facultad de Medicina, Universidad de Valencia, Valencia, Spain.
Universitat de València · ESINCLIVA Health Research Institute · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In inflammatory bowel disease (IBD), chronic inflammation in the gastrointestinal tract can lead to tissue damage and remodelling, which can ultimately result in fibrosis. Prolonged injury and inflammation can trigger the activation of fibroblasts and extracellular matrix (ECM) components. As fibrosis progresses, the tissue becomes increasingly stiff and less functional, which can lead to complications such as intestinal strictures, obstructive symptoms, and eventually, organ dysfunction. Epithelial cells play a key role in fibrosis, as they secrete cytokines and growth factors that promote fibroblast activation and ECM deposition. Additionally, epithelial cells can undergo a process called epithelial-mesenchymal transition, in which they acquire a more mesenchymal-like phenotype and contribute directly to fibroblast activation and ECM deposition. Overall, the interactions between epithelial cells, immune cells, and fibroblasts play a critical role in the development and progression of fibrosis in IBD. Understanding these complex interactions may provide new targets for therapeutic interventions to prevent or treat fibrosis in IBD. In this review, we have collected and discussed the recent literature highlighting the contribution of epithelial cells to the pathogenesis of the fibrotic complications of IBD, including evidence of EMT, the epigenetic control of the EMT, the potential influence of the intestinal microbiome in EMT, and the possible therapeutic strategies to target EMT. Finally we discuss the pro-fibrotic interactions epithelial-immune cells and epithelial-fibroblasts cells.

Indexed as

colitiscrohnepithelial cellsepithelial mesenchymal transitionfibrosisinflammatory bowel diseaseintestinal fibrosis

Identifiers

PMID37822869
PMCPMC10562728
OpenAlexW4387105705

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.