Evidence map›Paper›PMID 11890879›Full record

ReviewCurrent rheumatology reports2002

Connective tissue growth factor: a new and important player in the pathogenesis of fibrosis.

Andrew Leask, Alan Holmes, David J Abraham

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 212 citations in OpenAlex.

  1. Article
  2. Article
  3. Anoctamin-1 is induced by TGF-β and contributes to lung myofibroblast differentiation.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. CCN2/CTGF-A Modulator of the Optic Nerve Head Astrocyte.Frontiers in cell and developmental biology · 2022
    Article
  9. The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022
    Article
  10. The Immunogenetics of Morphea and Lichen Sclerosus.Advances in experimental medicine and biology · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cells, soluble factors and matrix harmonically play the concert of allograft integration.Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA · 2019
    Review
  18. Allograft tendons are a safe and effective option for revision ACL reconstruction: a clinical review.Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA · 2019
    Review
  19. Sustained Smad2 Phosphorylation Is Required for Myofibroblast Transformation in Response to TGF-β.American journal of respiratory cell and molecular biology · 2019
    Article
  20. Article
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

3 authors at 1 institution in 1 country.

Andrew LeaskCentre for Rheumatology, Department of Medicine, Royal Free and University College Medical School, Royal Free Campus, Rowland Hill St., London NW3 2PF, UK. d.abraham@rfc.ucl.ac.uk
Alan Holmes
David J Abraham
University College London · GB

Funding

RECOMBINANT HUMAN COLLAGEN &CTGF FOR TISSUE ENGINEERINGR01AR045879 · NIAMS · FIBROGEN, INC. · PI POLAREK, JAMES W · 1998 to 2002
$864k
NIAMS NIH HHS AR45879
6 · The paper itself

Abstract

Connective tissue fibrosis is the final common pathogenic process for almost all forms of chronic tissue injury. Whether caused by vascular dysfunction, inflammation, metabolic injury, trauma, or environmental agents, once initiated the fibrogenic process results in the progressive replacement of the normal tissue architecture with fibrotic lesions that eventually lead to organ compromise and failure. Fibrosis can be considered as a dysregulation in the normal tissue repair mechanism, resulting in severe tissue scarring. Fibrosis appears to be a consequence of linked processes, including the proliferation of resident fibroblast cell types, the increased production and deposition of extracellular matrix components, and the transition of fibroblasts into cells exhibiting a myofibroblast phenotype. Although transforming growth factor-beta (TGF beta) has long been regarded as a pivotal growth factor in the formation and maintenance of connective tissues and as a major driving influence in many progressive fibrotic diseases, attention has focused recently on the role of connective tissue growth factor (CTGF) in fibrosis. CTGF is selectively and rapidly induced in mesenchymally derived cells by the action of TGF beta. CTGF expression is increased in many fibrosing diseases. In addition, increasing evidence from in vivo and in vitro models of tissue remodeling and fibrosis suggest that CTGF may represent a downstream effector molecule of the profibrotic activities of TGF beta in the maintenance and repair of connective tissues and within fibrotic disease settings.

Indexed as

Intercellular Signaling Peptides and ProteinsAnimalsCarrier ProteinsConnective Tissue Growth FactorFibrosisGrowth SubstancesHumansImmediate-Early ProteinsMitogensScleroderma, SystemicCarrier ProteinsCCN2 protein, humanConnective Tissue Growth FactorGrowth SubstancesImmediate-Early ProteinsIntercellular Signaling Peptides and ProteinsMitogens

Identifiers

PMID11890879
OpenAlexW2029427032

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.