Evidence map›Paper›PMID 26729705›Full record

ArticleOncotarget2015

Oleoylethanolamide, an endogenous PPAR-α ligand, attenuates liver fibrosis targeting hepatic stellate cells.

Ling Chen, Long Li, Junde Chen, Lei Li, Zihan Zheng, Jie Ren, Yan Qiu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. The Role of Cannabidiol in Liver Disease: A Systemic Review.International journal of molecular sciences · 2024
    Pooled it
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  16. The role of PPAR in fungal keratitis.Frontiers in immunology · 2024
    Review
  17. Article
  18. Novel Curcumin Analogue L6H4 in Treating Liver Fibrosis and Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
    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

7 authors at 5 institutions in 2 countries.

Ling ChenDepartment of Medical Sciences, Medical College, Xiamen University, Xiamen, Fujian, China.
Long LiDepartment of Medical Sciences, Medical College, Xiamen University, Xiamen, Fujian, China.
Junde ChenMarine Biological Resource Comprehensive Utilization Engineering Research Center of The State Oceanic Administration, The Third Institute of Oceanography of The State Oceanic Administration, Xiamen, Fujian, China.
Lei LiDepartment of Medical Sciences, Medical College, Xiamen University, Xiamen, Fujian, China.
Zihan ZhengCollege of Arts and Sciences, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Jie RenDepartment of Medical Sciences, Medical College, Xiamen University, Xiamen, Fujian, China.
Yan QiuDepartment of Medical Sciences, Medical College, Xiamen University, Xiamen, Fujian, China.
First Affiliated Hospital of Xiamen University · CNXiamen University · CNFirst Affiliated Hospital of University of South China · CNFujian Institute of Oceanography · CNUniversity of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oleoylethanolamide (OEA), an endocannabinoid-like molecule, was revealed to modulate lipid metabolism through a peroxisome proliferator-activated receptor-α (PPAR-α) mediated mechanism. In present study, we further investigated the activities and mechanisms of OEA in ameliorating hepatic fibrosis in Sv/129 mice induced by a methionine choline-deficient (MCD) diet or thioacetamide (TAA) treatment. Liver fibrosis development was assessed by Hematoxylin-eosin and Sirius red staining. Treatment with OEA (5 mg/kg/day, intraperitoneal injection, i.p.) significantly attenuated the progress of liver fibrosis in both two experimental animal models by blocking the activation of hepatic stellate cells (HSCs). Gene expression analysis of hepatic tissues indicated that OEA inhibited the expression of α-smooth muscle action (α-SMA) and collagen matrix, fibrosis markers, and genes involved in inflammation and extracellular matrix remodeling. In vitro studies showed that OEA inhibited transforming growth factor β1-stimulated HSCs activation through suppressing Smad2/3 phosphorylation, α-SMA expression and myofibroblast transformation. These improvements could not be observed in PPAR-α knockout mice models with OEA administration, which suggested all the anti-fibrotic effects of OEA in vivo and in vitro were mediated by PPAR-α activation. Collectively, our results suggested that OEA exerted a pharmacological effect on modulating hepatic fibrosis development through the inhibition of HSCs activation in liver and therefore may be a potential therapeutic agent for liver fibrosis.

Indexed as

AnimalsBlotting, WesternDisease Models, AnimalEndocannabinoidsFluorescent Antibody TechniqueHepatic Stellate CellsLigandsLiver CirrhosisMiceMice, 129 StrainMice, KnockoutOleic AcidsPPAR alphaReal-Time Polymerase Chain ReactionEndocannabinoidsLigandsOleic AcidsoleoylethanolamidePPAR alphahepatic stellate cellsliver fibrosisOEAPathology SectionPPAR-αTGF-β1

Identifiers

PMID26729705
PMCPMC4767450
OpenAlexW2182271660

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.