Evidence map›Paper›PMID 19713852›Full record

ReviewCurrent opinion in rheumatology2009

Noncanonical transforming growth factor beta signaling in scleroderma fibrosis.

Maria Trojanowska

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Comparative proteomics reveals elevated CCN2 in NGLY1-deficient cells.Biochemical and biophysical research communications · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Role of macrophage TRPV4 in inflammation.Laboratory investigation; a journal of technical methods and pathology · 2020
    Review
  13. Article
  14. Article
  15. TRPV4 ion channel is a novel regulator of dermal myofibroblast differentiation.American journal of physiology. Cell physiology · 2017
    Article
  16. Article
  17. Article
  18. Functional autoantibodies in systemic sclerosis.Seminars in immunopathology · 2015
    Review
  19. Yin and Yang revisited: CCN3 as an anti-fibrotic therapeutic?Journal of cell communication and signaling · 2015
    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

1 author at 1 institution in 1 country.

Maria TrojanowskaDivision of Rheumatology and Immunology, Medical University of South Carolina, Charleston, South Carolina 29425, USA. trojanme@musc.edu
Medical University of South Carolina · US

Funding

The molecular mechanisms of fibrosisR01AR042334 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1994 to 2018
$5.2M
TGF BETA RECEPTOR SIGNALING IN SCLERODERMAR01AR044883 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1998 to 2012
$3.3M
NIAMS NIH HHS R01 AR042334NIAMS NIH HHS R01 AR044883
6 · The paper itself

Abstract

purpose of reviewPersistent transforming growth factor beta (TGF-beta) signaling is the major factor contributing to scleroderma (SSc) fibrosis. This review will summarize recent progress on the noncanonical TGF-beta signaling pathways and their role in SSc fibrosis. RECENT

findingsCanonical TGF-beta signaling involves activation of the TGF-beta receptors and downstream signal transducers Smad2/3. The term noncanonical TGF-beta signaling includes a variety of intracellular signaling pathways activated by TGF-beta independently of Smad2/3 activation. There is evidence that these pathways play important role in SSc fibrosis. In a subset of SSc fibroblasts, a multiligand receptor complex consisting of TGF-beta and CCN2 receptors drives constitutive activation of the Smad1 pathway. CCN2 is also a primary effector of this pathway, thus establishing an autocrine loop that amplifies TGF-beta signaling. SSc fibroblasts also demonstrate reduced expression of endogenous antagonists of TGF-beta signaling including transcriptional repressors, Friend leukemia integration-1 and perixosome proliferator-activated receptor-gamma, as well as inhibitor of Smad3 phosphorylation, PTEN. PTEN is a key mediator of the cross-talk between the sphingosine kinase and the TGF-beta pathways. SUMMARY: Discovery of the role of noncanonical TGF-beta signaling in fibrosis offers new molecular targets for the antifibrotic therapies. Due to the heterogeneous nature of SSc, knowledge of these pathways could help to tailor the therapy to the individual patient depending on the activation status of a specific profibrotic pathway.

Indexed as

AnimalsAutocrine CommunicationCollagenConnective Tissue Growth FactorFibrosisHumansModels, BiologicalPhosphotransferases (Alcohol Group Acceptor)PTEN PhosphohydrolaseScleroderma, SystemicSignal TransductionSmad1 ProteinSphingosine KinaseTransforming Growth Factor betaCCN2 protein, humanCollagenConnective Tissue Growth FactorPhosphotransferases (Alcohol Group Acceptor)PTEN PhosphohydrolasePTEN protein, humanSmad1 ProteinSMAD1 protein, humanSphingosine KinaseTransforming Growth Factor beta

Identifiers

PMID19713852
PMCPMC4020352
OpenAlexW2091708232

What OpenQuestion holds

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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.