Evidence map›Paper›PMID 28422956›Full record

ArticlePloS one2017

Chronic activation of PPARα with fenofibrate reduces autophagic proteins in the liver of mice independent of FGF21.

Eunjung Jo, Songpei Li, Qingning Liang, Xinmei Zhang, Hao Wang, Terence P Herbert, Trisha A Jenkins, Aimin Xu, Ji-Ming Ye

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

2 citing papers in PubMed, 27 citations in OpenAlex.

  1. Autophagic Regulation of p62 is Critical for Cancer Therapy.International journal of molecular sciences · 2018
    Review
  2. Anticancer activity of salicin and fenofibrate.Naunyn-Schmiedeberg's archives of pharmacology · 2017
    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

9 authors at 2 institutions in 2 countries.

Eunjung JoSchool of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia.
Songpei LiSchool of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia.
Qingning LiangState Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, Hong Kong University, Hong Kong, China.
Xinmei ZhangSchool of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia.
Hao WangSchool of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia.
Terence P HerbertSchool of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia.
Trisha A JenkinsSchool of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia.
Aimin XuState Key Laboratory of Pharmaceutical Biotechnology, Department of Medicine, Hong Kong University, Hong Kong, China.
Ji-Ming YeSchool of Health and Biomedical Sciences, RMIT University, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0003-3983-0098
RMIT University · AUUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a catabolic mechanism to degrade cellular components to maintain cellular energy levels during starvation, a condition where PPARα may be activated. Here we report a reduced autophagic capacity in the liver following chronic activation of PPARα with fenofibrate (FB) in mice. Chronic administration of the PPARα agonist FB substantially reduced the levels of multiple autophagy proteins in the liver (Atg3, Agt4B, Atg5, Atg7 and beclin 1) which were associated with a decrease in the light chain LC3II/LC3I ratio and the accumulation of p62. This was concomitant with an increase in the expression of lipogenic proteins mSREBP1c, ACC, FAS and SCD1. These effects of FB were completely abolished in PPARα-/- mice but remained intact in mice with global deletion of FGF21, a key downstream mediator for PPARα-induced effects. Further studies showed that decreased the content of autophagy proteins by FB was associated with a significant reduction in the level of FoxO1, a transcriptional regulator of autophagic proteins, which occurred independently of both mTOR and Akt. These findings suggest that chronic stimulation of PPARα may suppress the autophagy capacity in the liver as a result of reduced content of a number of autophagy-associated proteins independent of FGF21.

Indexed as

AnimalsAutophagyAutophagy-Related Protein 5Autophagy-Related Protein 7Autophagy-Related ProteinsBeclin-1Blood GlucoseCysteine Endopeptidasesfas ReceptorFenofibrateFibroblast Growth FactorsForkhead Box Protein O1Gene Expression RegulationLiverMiceMice, Inbred C57BLAtg3 protein, mouseAtg4b protein, mouseAtg5 protein, mouseAtg7 protein, mouseAutophagy-Related Protein 5Autophagy-Related Protein 7Autophagy-Related ProteinsBeclin-1Becn1 protein, mouseBlood GlucoseCysteine EndopeptidasesFas protein, mousefas ReceptorFenofibratefibroblast growth factor 21Fibroblast Growth FactorsForkhead Box Protein O1Foxo1 protein, mouseMap1lc3b protein, mouseMicrotubule-Associated ProteinsmTOR protein, mousePPAR alphaProto-Oncogene Proteins c-aktScd1 protein, mouseSequestosome-1 ProteinSqstm1 protein, mouseSrebf1 protein, mouseStearoyl-CoA DesaturaseSterol Regulatory Element Binding Protein 1TOR Serine-Threonine KinasesTriglyceridesUbiquitin-Conjugating Enzymes

Identifiers

PMID28422956
PMCPMC5396863
OpenAlexW2605808009

What OpenQuestion holds

Textmetadata
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.