Evidence map›Paper›PMID 23063463›Full record

ReviewCellular signalling2013

TGF-β signaling in tissue fibrosis: redox controls, target genes and therapeutic opportunities.

Rohan Samarakoon, Jessica M Overstreet, Paul J Higgins

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed
9.0field-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

189 citing papers in PubMed, 327 citations in OpenAlex.

  1. Improvement in Hepatic Fibrosis Biomarkers Associated With Chemokine Receptor Inactivation Through Mutation or Therapeutic Blockade.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2019
    Trial
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Anti-fibrotic effect ofFrontiers in bioengineering and biotechnology · 2026
    Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Angiogenesis: Biological Mechanisms and In Vitro Models.Annals of biomedical engineering · 2025
    Review
  19. Article
  20. Article

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

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.

Rohan SamarakoonCenter for Cell Biology and Cancer Research, Albany Medical College, 47 New Scotland Avenue, Albany, NY 12208, USA.
Jessica M Overstreet
Paul J Higgins
Albany Medical Center Hospital · US

Funding

MATRIX MEDIATORS OF WOUND HEALINGR01GM057242 · NIGMS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI HIGGINS, PAUL J. · 1998 to 2010
$3.2M
NIGMS NIH HHS GM057242NIGMS NIH HHS R01 GM057242
6 · The paper itself

Abstract

During development of TGF-β1-initiated fibroproliferative disorders, NADPH oxidases (NOX family members) generate reactive oxygen species (ROS) resulting in downstream transcription of a subset genes encoding matrix structural elements and profibrotic factors. Prominent among the repertoire of disease-implicated genes is the TGF-β1 target gene encoding the potent profibrotic matricellular protein plasminogen activator inhibitor-1 (PAI-1 or SERPINE1). PAI-1 is the major physiologic inhibitor of the plasmin-based pericellular cascade and a causative factor in the development of vascular thrombotic and fibroproliferative disorders. ROS generation in response to TGF-β1 stimulation is rapid and precedes PAI-1 induction; engagement of non-SMAD (e.g., EGFR, Src kinase, MAP kinases, p53) and SMAD2/3 pathways are both required for PAI-1 expression and are ROS-dependent. Recent findings suggest a novel role for p53 in TGF-β1-induced PAI-1 transcription that involves ROS generation and p53/SMAD interactions. Targeting ROS and ROS-activated cellular events is likely to have therapeutic implications in the management of fibrotic disorders, particularly in the context of prolonged TGF-β1 signaling.

Indexed as

Signal TransductionErbB ReceptorsFibrosisHumansNADPH OxidasesOxidation-ReductionPlasminogen Activator Inhibitor 1Reactive Oxygen SpeciesSmad2 ProteinSmad3 ProteinTransforming Growth Factor betaTumor Suppressor Protein p53ErbB ReceptorsNADPH OxidasesPlasminogen Activator Inhibitor 1Reactive Oxygen SpeciesSmad2 ProteinSmad3 ProteinTransforming Growth Factor betaTumor Suppressor Protein p53

Identifiers

PMID23063463
PMCPMC3508263
OpenAlexW2009358874

What OpenQuestion holds

Textmetadata
LicenceTDM
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.