Evidence map›Paper›PMID 27538444›Full record

ArticleGut and liver2017

Elk-3 Contributes to the Progression of Liver Fibrosis by Regulating the Epithelial-Mesenchymal Transition.

Tian Zhu Li, Sung Min Kim, Wonhee Hur, Jung Eun Choi, Jung-Hee Kim, Sung Woo Hong, Eun Byul Lee, Joon Ho Lee, Seung Kew Yoon

Open access · diamondAbstract read
In one paragraph

Article in Gut and liver, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

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  13. [Expression characteristics and functional analysis of ELK3 in gastric cancer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 2 countries.

Tian Zhu LiThe Catholic University Liver Research Center & WHO Collaborating Center of Viral Hepatitis, The Catholic University of Korea College of Medicine, Seoul, Korea.
Sung Min KimThe Catholic University Liver Research Center & WHO Collaborating Center of Viral Hepatitis, The Catholic University of Korea College of Medicine, Seoul, Korea.
Wonhee HurThe Catholic University Liver Research Center & WHO Collaborating Center of Viral Hepatitis, The Catholic University of Korea College of Medicine, Seoul, Korea.
Jung Eun ChoiThe Catholic University Liver Research Center & WHO Collaborating Center of Viral Hepatitis, The Catholic University of Korea College of Medicine, Seoul, Korea.
Jung-Hee KimThe Catholic University Liver Research Center & WHO Collaborating Center of Viral Hepatitis, The Catholic University of Korea College of Medicine, Seoul, Korea.
Sung Woo HongThe Catholic University Liver Research Center & WHO Collaborating Center of Viral Hepatitis, The Catholic University of Korea College of Medicine, Seoul, Korea.
Eun Byul LeeThe Catholic University Liver Research Center & WHO Collaborating Center of Viral Hepatitis, The Catholic University of Korea College of Medicine, Seoul, Korea.
Joon Ho LeeThe Catholic University Liver Research Center & WHO Collaborating Center of Viral Hepatitis, The Catholic University of Korea College of Medicine, Seoul, Korea.
Seung Kew YoonThe Catholic University Liver Research Center & WHO Collaborating Center of Viral Hepatitis, The Catholic University of Korea College of Medicine, Seoul, Korea.
Catholic University of Korea · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsThe role of Elk-3 in the epithelial-mesenchymal transition (EMT) during liver fibrogenesis remains unclear. Here, we determined the expression of Elk-3 in

methodsWe established an

resultsThe expression levels of mesenchymal markers were increased during TGF-β1-induced EMT of hepatocytes. The expression levels of Elk-3 and Egr-1 were significantly (p<0.05) increased during the EMT of hepatocytes, in CCl₄-induced mouse liver fibrotic tissues, and in human liver cirrhotic tissues. Silencing of Elk-3 and inhibition of the Ras-Elk-3 pathway with an inhibitor suppressed the expression of EMT-related markers. Moreover, Elk-3 expression was regulated by p38 MAPK phosphorylation during EMT.

conclusionsElk-3 contributes to the progression of liver fibrosis by modulating the EMT via the regulation of Egr-1 under MAPK signaling.

Indexed as

ActinsAnimalsAntigens, CDBlotting, WesternCadherinsCarbon TetrachlorideCdh1 ProteinsCell LineDisease Models, AnimalEarly Growth Response Protein 1Epithelial-Mesenchymal TransitionGene Knockdown TechniquesHepatocytesHumansLiver CirrhosisMiceActinsalpha-smooth muscle actin, mouseAntigens, CDCadherinsCarbon TetrachlorideCDH1 protein, humanCdh1 ProteinsEarly Growth Response Protein 1Egr1 protein, mouseElk3 protein, mouseFzr1 protein, mouseMitogen-Activated Protein KinasesPiperazinesProto-Oncogene Proteins c-etsPyrazolesRNA, Small InterferingTransforming Growth Factor beta1VimentinXRP44X compoundEarly growth response-1Elk-3Epithelial-mesenchymal transitionLiver cirrhosisMAPK pathway

Identifiers

PMID27538444
PMCPMC5221867
OpenAlexW2508362181

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.