Evidence map›Paper›PMID 17589920›Full record

ReviewWorld journal of gastroenterology2007

Transforming growth factor-beta and fibrosis.

Franck Verrecchia, Alain Mauviel

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
237citing papers in PubMed, 1 pooled it
10.5field-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

237 citing papers in PubMed, 1 synthesis or guideline pooled it, 497 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Erythropoietin and Ferulic Acid Loaded on FeApplied biochemistry and biotechnology · 2026
    Article
  7. Inflammatory bowel disease and extracellular matrix: when victim becomes double agent.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  8. Antifibrotic Effects ofInternational journal of molecular sciences · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Antifibrotic and anti-inflammatory properties of halofuginone in a rat craniectomy model.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Physical Exercise: A Promising Treatment Against Organ Fibrosis.International journal of molecular sciences · 2025
    Review
  20. Review

177 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Franck VerrecchiaINSERM U697, Hopital Saint-Louis, Pavillon Bazin, 1 avenue Claude Vellefaux, Paris 75010, France. franck.verrecchia@stlouis.inserm.fr
Alain Mauviel
Inserm · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-beta (TGF-beta), a prototype of multifunctional cytokine, is a key regulator of extracellular matrix (ECM) assembly and remodeling. Specifically, TGF-beta isoforms have the ability to induce the expression of ECM proteins in mesenchymal cells, and to stimulate the production of protease inhibitors that prevent enzymatic breakdown of the ECM. Elevated TGF-beta expression in affected organs, and subsequent deregulation of TGF-beta functions, correlates with the abnormal connective tissue deposition observed during the onset of fibrotic diseases. During the last few years, tremendous progress has been made in the understanding of the molecular aspects of intracellular signaling downstream of the TGF-beta receptors. In particular, Smad proteins, TGF-beta receptor kinase substrates that translocate into the cell nucleus to act as transcription factors, have been studied extensively. The role of Smad3 in the transcriptional regulation of type I collagen gene expression and in the development of fibrosis, demonstrated both in vitro and in animal models with a targeted deletion of Smad3, is of critical importance because it may lead to novel therapeutic strategies against these diseases. This review focuses on the mechanisms underlying Smad modulation of fibrillar collagen expression and how it relates to fibrotic processes.

Indexed as

AnimalsCollagenConnective TissueConnective Tissue Growth FactorExtracellular MatrixFibrosisHumansImmediate-Early ProteinsIntercellular Signaling Peptides and ProteinsReceptors, Transforming Growth Factor betaSkinSkin DiseasesSmad ProteinsTransforming Growth Factor betaCCN2 protein, humanCollagenConnective Tissue Growth FactorImmediate-Early ProteinsIntercellular Signaling Peptides and ProteinsReceptors, Transforming Growth Factor betaSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID17589920
PMCPMC4172611
OpenAlexW201653061

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.