Evidence map›Paper›PMID 25108224›Full record

ArticleThe American journal of pathology2014

Transforming growth factor-β-independent role of connective tissue growth factor in the development of liver fibrosis.

Keiko Sakai, Safdar Jawaid, Takako Sasaki, George Bou-Gharios, Takao Sakai

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 28 citations in OpenAlex.

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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

5 authors at 3 institutions in 3 countries.

Keiko SakaiMRC Centre for Drug Safety Science, Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom; Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Safdar JawaidDepartment of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Takako SasakiDepartment of Biochemistry, Faculty of Medicine, Oita University, Oita, Japan.
George Bou-GhariosDepartment of Musculoskeletal Biology, Institute of Aging and Chronic Disease, University of Liverpool, Liverpool, United Kingdom.
Takao SakaiMRC Centre for Drug Safety Science, Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom; Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio. Electronic address: sakait@liverpool.ac.uk.
University of Liverpool · GBCleveland Clinic Lerner College of Medicine · USOita University · JP

Funding

Fibronectin deposition and TGF-beta activation in liver fibrosisR01DK074538 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI SAKAI, TAKAO · 2007 to 2011
$1.5M
Medical Research Council MR/K006312/1NIDDK NIH HHS DK074538NIDDK NIH HHS R01 DK074538
6 · The paper itself

Abstract

We previously identified transforming growth factor (TGF)-β signaling as a fibronectin-independent mechanism of type I collagen fibrillogenesis following adult liver injury. To address the contribution of TGF-β signaling during the development of liver fibrosis, we generated adult mice lacking TGF-β type II receptor (TGF-βIIR) from the liver. TGF-βIIR knockout livers indeed showed a dominant effect in reducing fibrosis, but fibrosis still remained approximately 45% compared with control and fibronectin knockout livers. Unexpectedly, this was accompanied by significant up-regulation of connective tissue growth factor mRNA levels. Organized type I collagen networks in TGF-βIIR knockout livers colocalized well with fibronectin. We provide evidence that elimination of TGF-βIIR is not sufficient to completely prevent liver fibrosis. Our results indicate a TGF-β-independent mechanism of type I collagen production and suggest connective tissue growth factor as its potent mediator. We advocate combined elimination of TGF-β signaling and connective tissue growth factor as a potential therapeutic target by which to attenuate liver fibrosis.

Indexed as

Gene Expression RegulationSignal TransductionAnimalsCarbon TetrachlorideChronic DiseaseCollagen Type IConnective Tissue Growth FactorDisease Models, AnimalFibronectinsHumansLiverLiver CirrhosisMiceMice, KnockoutProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaCarbon TetrachlorideCCN2 protein, mouseCollagen Type IConnective Tissue Growth FactorFibronectinsProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIRNA, MessengerTransforming Growth Factor beta

Identifiers

PMID25108224
PMCPMC4715221
OpenAlexW2117798650

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.