Evidence map›Paper›PMID 12622414›Full record

ReviewInternational journal of gastrointestinal cancer2002

TGFbeta-induced fibrogenesis of the pancreas.

Andre Menke, Guido Adler

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of gastrointestinal cancer, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

26 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. ROS and TGFβ: from pancreatic tumour growth to metastasis.Journal of experimental & clinical cancer research : CR · 2021
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Carcinogenesis of pancreatic adenocarcinoma: precursor lesions.International journal of molecular sciences · 2013
    Review
  10. Prolonged high fat/alcohol exposure increases TRPV4 and its functional responses in pancreatic stellate cells.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  11. Article
  12. Article
  13. Matrix metalloproteinase-9, transforming growth factor-β1, and tumor necrosis factor-α plasma levels in chronic pancreatitis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2013
    Article
  14. Review
  15. Article
  16. Plasma TGF-β1, MMP-1 and MMP-3 Levels in Chronic Pancreatitis.Indian journal of clinical biochemistry : IJCB · 2012
    Article
  17. Review
  18. Article
  19. Article
  20. Protective role of angiotensin II type 2 receptor signaling in a mouse model of pancreatic fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2009
    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

2 authors at 1 institution in 1 country.

Andre MenkeDepartment of Internal Medicine I, University of Ulm, Robert-Koch-Strasse 8, D-89070 Ulm, Germany. andre.menke@medizin.uni-ulm.de
Guido Adler
Universität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biological cause of fibrosis is the accumulation of excessive amounts of extracellular matrix (ECM) which leads to tissue dysfunction and organ failure. A strong correlation can be found between pancreatic diseases and fibrotic processes, in particular chronic pancreatitis and pancreatic cancer. There is growing evidence that pancreatic fibrosis represents a dysregulation of the normal repair processes after injury. This concept is based on the findings that fibrosis and tissue repair involve similar biological reactions regulated by the same group of molecules. The best characterized example for these regulatory molecules are the members of the transforming growth factor beta family (TGFbeta). TGFbeta1 represents the prototype of this family of highly similar growth factors, with the unique ability to stimulate the expression and deposition of extracellular matrix and to inhibit its degradation. Growth factor-induced fibrotic events are targeted by a myofibroblast-like cell called pancreatic stellate cell (PSC). These cells show enhanced expression of all-important ECM proteins after TGFbeta stimulation including collagen, fibronectin and proteoglycans. At the same time TGFbeta inhibits the degradation of ECM by blocking the secretion of proteases and stimulating the production of naturally occurring protease inhibitors.

Indexed as

CollagenEndopeptidasesExtracellular MatrixFibrosisHumansPancreatic NeoplasmsTransforming Growth Factor betaCollagenEndopeptidasesTransforming Growth Factor beta

Identifiers

PMID12622414
OpenAlexW2054041390

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.