Evidence map›Paper›PMID 25253939›Full record

ReviewWorld journal of gastroenterology2014

Smad3 phospho-isoform signaling in hepatitis C virus-related chronic liver diseases.

Takashi Yamaguchi, Katsunori Yoshida, Miki Murata, Koichi Matsuzaki

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. Astragaloside IV suppresses migration and invasion of TGF-βNaunyn-Schmiedeberg's archives of pharmacology · 2022
    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

4 authors at 1 institution in 1 country.

Takashi YamaguchiTakashi Yamaguchi, Katsunori Yoshida, Miki Murata, Koichi Matsuzaki, Department of Gastroenterology and Hepatology, Kansai Medical University, Osaka 570-8506, Japan.
Katsunori YoshidaTakashi Yamaguchi, Katsunori Yoshida, Miki Murata, Koichi Matsuzaki, Department of Gastroenterology and Hepatology, Kansai Medical University, Osaka 570-8506, Japan.
Miki MurataTakashi Yamaguchi, Katsunori Yoshida, Miki Murata, Koichi Matsuzaki, Department of Gastroenterology and Hepatology, Kansai Medical University, Osaka 570-8506, Japan.
Koichi MatsuzakiTakashi Yamaguchi, Katsunori Yoshida, Miki Murata, Koichi Matsuzaki, Department of Gastroenterology and Hepatology, Kansai Medical University, Osaka 570-8506, Japan.
Sekisui Medical (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The risk of hepatocellular carcinoma (HCC) development increases as hepatitis virus C (HCV)-related liver diseases progress, especially in patients with active inflammation. Insight into hepatic carcinogenesis have emerged from recent detailed analyses of transforming growth factor-β and c-Jun-N-terminal kinase signaling processes directed by multiple phosphorylated (phospho)-isoforms of a Smad3 mediator. In the course of HCV-related chronic liver diseases, chronic inflammation and host genetic/epigenetic alterations additively shift the hepatocytic Smad3 phospho-isoform signaling from tumor suppression to carcinogenesis, increasing the risk of HCC. Chronic inflammation represents an early carcinogenic step that provides a nonmutagenic tumor-promoting stimulus. After undergoing successful antiviral therapy, patients with chronic hepatitis C could experience a lower risk of HCC as Smad3 phospho-isoform signaling reverses from potential carcinogenesis to tumor suppression. Even after HCV clearance, however, patients with cirrhosis could still develop HCC because of sustained, intense carcinogenic Smad3 phospho-isoform signaling that is possibly caused by genetic or epigenetic alterations. Smad3 phospho-isoforms should assist with evaluating the effectiveness of interventions aimed at reducing human HCC.

Indexed as

Signal TransductionAnimalsAntiviral AgentsCarcinoma, HepatocellularCell Transformation, ViralHepacivirusHepatitis C, ChronicHost-Pathogen InteractionsHumansJNK Mitogen-Activated Protein KinasesLiverLiver CirrhosisLiver NeoplasmsPhosphorylationProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaAntiviral AgentsJNK Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ISmad3 ProteinChronic inflammationc-Jun N-terminal kinaseHepatitis C virusHepatocellular carcinomaSmad3 phospho-isoform signalingTransforming growth factor β

Identifiers

PMID25253939
PMCPMC4168072
OpenAlexW1975329267

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.