Evidence map›Paper›PMID 25050845›Full record

ReviewInternational journal of oncology2014

TGF-β/Smad signaling during hepatic fibro-carcinogenesis (review).

Katsunori Yoshida, Miki Murata, Takashi Yamaguchi, Koichi Matsuzaki

Open access · hybridAbstract readReview
In one paragraph

Review in International journal of oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 127 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. MST1/2 DKO abates salvianolic acid B's therapeutic effect on CClNaunyn-Schmiedeberg's archives of pharmacology · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Anti-Fibrotic Effect of Oleamide Identified from theInternational journal of molecular sciences · 2025
    Article
  13. Article
  14. Role of microRNA-363 during tumor progression and invasion.Journal of physiology and biochemistry · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

11 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

4 authors at 1 institution in 1 country.

Katsunori YoshidaDepartment of Gastroenterology and Hepatology, Kansai Medical University, Hirakata, Osaka 573-1010, Japan.
Miki MurataDepartment of Gastroenterology and Hepatology, Kansai Medical University, Hirakata, Osaka 573-1010, Japan.
Takashi YamaguchiDepartment of Gastroenterology and Hepatology, Kansai Medical University, Hirakata, Osaka 573-1010, Japan.
Koichi MatsuzakiDepartment of Gastroenterology and Hepatology, Kansai Medical University, Hirakata, Osaka 573-1010, Japan.
Kansai Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

After hepatitis virus infection, plasma transforming growth factor (TGF)-β increases in either the acute or chronic inflammatory microenvironment. Although TGF-β is upregulated in patients with hepatocellular carcinoma, it is one of the most potent growth inhibitors for hepatocytes. This cytokine also upregulates extracellular matrix (ECM) production of hepatic stellate cells. Therefore, TGF-β is considered to be the major factor regulating liver carcinogenesis and accelerating liver fibrosis. Smad2 and Smad3 act as the intracellular mediators of TGF-β signal transduction pathway. We have generated numerous antibodies against individual phosphorylation sites in Smad2/3, and identified 3 types of phosphorylated forms (phospho-isoforms): COOH-terminally phosphorylated Smad2/3 (pSmad2C and pSmad3C), linker phosphorylated Smad2/3 (pSmad2L and pSmad3L) and dually phosphorylated Smad2/3 (pSmad2L/C and pSmad3L/C). These Smad phospho-isoforms are categorized into 3 groups: cytostatic pSmad3C signaling, mitogenic pSmad3L signaling and invasive/fibrogenic pSmad2L/C signaling. In this review, we describe differential regulation of TGF-β/Smad signaling after acute or chronic liver injuries. In addition, we consider how chronic inflammation associated with hepatitis virus infection promotes hepatic fibrosis and carcinogenesis (fibro-carcinogenesis), focusing on alteration of Smad phospho-isoform signaling. Finally, we show reversibility of Smad phospho-isoform signaling after therapy against hepatitis virus infection.

Indexed as

Signal TransductionAnimalsGene Expression RegulationGene Expression Regulation, NeoplasticHepatitis, Viral, HumanHumansLiver DiseasesPhosphorylationSmad ProteinsTransforming Growth Factor betaSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID25050845
PMCPMC4151811
OpenAlexW2093619650

What OpenQuestion holds

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LicenceCC BY
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.