Evidence map›Paper›PMID 28646549›Full record

ArticleBritish journal of pharmacology2017

Inhibition of JNK signalling mediates PPARα-dependent protection against intrahepatic cholestasis by fenofibrate.

Manyun Dai, Julin Yang, Minzhu Xie, Jiao Lin, Min Luo, Huiying Hua, Gangming Xu, Hante Lin, Danjun Song, Yuqing Cheng and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 49 citations in OpenAlex.

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  9. Review
  10. Down-regulation of hepatic CLOCK by PPARα is involved in inhibition of NAFLD.Journal of molecular medicine (Berlin, Germany) · 2023
    Article
  11. Article
  12. Review
  13. Article
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  17. Observational
  18. Hepatocyte peroxisome proliferator-activated receptor α regulates bile acid synthesis and transport.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    Article
  19. Article
  20. 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

14 authors at 4 institutions in 3 countries.

Manyun DaiMedical School of Ningbo University, Ningbo, China.ORCID http://orcid.org/0000-0002-7184-5129
Julin YangNingbo College of Health Sciences, Ningbo, China.
Minzhu XieMedical School of Ningbo University, Ningbo, China.
Jiao LinMedical School of Ningbo University, Ningbo, China.
Min LuoMedical School of Ningbo University, Ningbo, China.
Huiying HuaMedical School of Ningbo University, Ningbo, China.
Gangming XuMedical School of Ningbo University, Ningbo, China.
Hante LinMedical School of Ningbo University, Ningbo, China.
Danjun SongMedical School of Ningbo University, Ningbo, China.
Yuqing ChengHunan Normal University, Changsha, China.
Bin GuoHunan Normal University, Changsha, China.
Jinshun ZhaoMedical School of Ningbo University, Ningbo, China.
Frank J GonzalezLaboratory of Metabolism, National Cancer Institute, NIH, Bethesda, MD, USA.
Aiming LiuMedical School of Ningbo University, Ningbo, China.
Ningbo University · CNHunan Normal University · CNNational Cancer Institute · USUniversity of Bahrain · BH

Funding

Xenobiotic receptorsZIABC005562 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$26.9M
6 · The paper itself

Abstract

background and purposeFenofibrate, a PPARα agonist, is the most widely prescribed drug for treating hyperlipidaemia. Although fibrate drugs are reported to be beneficial for cholestasis, their underlying mechanism has not been determined. EXPERIMENTAL APPROACH: Wild-type mice and Pparα-null mice were pretreated orally with fenofibrate for 3 days, following which α-naphthylisothiocyanate (ANIT) was administered to induce cholestasis. The PPARα agonist WY14643 and JNK inhibitor SP600125 were used to determine the role of PPARα and the JNK pathway, respectively, in cholestatic liver injury. The same fenofibrate regimen was applied to investigate its beneficial effects on sclerosing cholangitis in a DDC-induced cholestatic model. KEY

resultsFenofibrate, 25 mg·kg CONCLUSIONS AND IMPLICATIONS: These data suggest that the protective effects of fenofibrate against cholestasis-induced hepatic injury are dependent on PPARα and fenofibrate dose, and are mediated through inhibition of JNK signalling. This mechanism of fenofibrate protection against intrahepatic cholestasis may offer additional therapeutic opportunities for cholestatic liver diseases.

Indexed as

1-NaphthylisothiocyanateAnimalsAnthracenesCholestasis, IntrahepaticDose-Response Relationship, DrugFenofibrateJNK Mitogen-Activated Protein KinasesMiceMice, KnockoutPPAR alphaProtein Kinase InhibitorsPyrimidinesSignal TransductionStructure-Activity Relationship1-NaphthylisothiocyanateAnthracenesFenofibrateJNK Mitogen-Activated Protein Kinasespirinixic acidPPAR alphaProtein Kinase InhibitorspyrazolanthronePyrimidines

Identifiers

PMID28646549
PMCPMC5573431
OpenAlexW2703188572

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.