Evidence map›Paper›PMID 24351808›Full record

ArticleInternational journal of molecular sciences2013

EZH2 down-regulation exacerbates lipid accumulation and inflammation in in vitro and in vivo NAFLD.

Serena Vella, Daniela Gnani, Annalisa Crudele, Sara Ceccarelli, Cristiano De Stefanis, Stefania Gaspari, Valerio Nobili, Franco Locatelli, Victor E Marquez, Rossella Rota and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Targeting the Liver Serine Protease TMPRSS6 Ameliorates Steatosis and Attenuates Fibrosis in Experimental MASLD.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Article
  4. Review
  5. Histone Modifications in NAFLD: Mechanisms and Potential Therapy.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. EZH2 as a Potential Target for NAFLD Therapy.International journal of molecular sciences · 2020
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  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

11 authors at 3 institutions in 2 countries.

Serena Vella
Daniela Gnani
Annalisa Crudele
Sara Ceccarelli
Cristiano De Stefanis
Stefania Gaspari
Valerio Nobili
Franco Locatelli
Victor E Marquez
Rossella RotaDepartment of Oncohematology, Bambino Gesù Children's Hospital, IRCCS, Rome 00165, Italy. rossella.rota@opbg.net.
Anna AlisiDepartment of Oncohematology, Bambino Gesù Children's Hospital, IRCCS, Rome 00165, Italy. anna.alisi@opbg.net.
Bambino Gesù Children's Hospital · ITFrederick National Laboratory for Cancer Research · USUniversity of Pavia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent, chronic liver diseases, worldwide. It is a multifactorial disease caused by complex interactions between genetic, epigenetic and environmental factors. Recently, several microRNAs, some of which epigenetically regulated, have been found to be up- and/or down-regulated during NAFLD development. However, in NAFLD, the essential role of the Polycomb Group protein Enhancer of Zeste Homolog 2 (EZH2), which controls the epigenetic silencing of specific genes and/or microRNAs by trimethylating Lys27 on histone H3, still remains unknown. In this study, we demonstrate that the nuclear expression/activity of the EZH2 protein is down-regulated both in livers from NAFLD rats and in the free fatty acid-treated HepG2. The drop in EZH2 is inversely correlated with: (i) lipid accumulation; (ii) the expression of pro-inflammatory markers including TNF-α and TGF-β; and (iii) the expression of miR-200b and miR-155. Consistently, the pharmacological inhibition of EZH2 by 3-Deazaneplanocin A (DZNep) significantly reduces EZH2 expression/activity, while it increases lipid accumulation, inflammatory molecules and microRNAs. In conclusion, the results of this study suggest that the defective activity of EZH2 can enhance the NAFLD development by favouring steatosis and the de-repression of the inflammatory genes and that of specific microRNAs.

Indexed as

Down-RegulationAdenosineAnimalsDisease Models, AnimalEnhancer of Zeste Homolog 2 ProteinFatty LiverHep G2 CellsHistonesHumansMicroRNAsNon-alcoholic Fatty Liver DiseaseOleic AcidPalmitic AcidPolycomb Repressive Complex 2RatsRats, Sprague-Dawley3-deazaneplanocinAdenosineEnhancer of Zeste Homolog 2 ProteinEZH2 protein, ratHistonesMicroRNAsMIRN155 microRNA, ratMIRN200 microRNA, ratOleic AcidPalmitic AcidPolycomb Repressive Complex 2RNA, MessengerTransforming Growth Factor betaTumor Necrosis Factor-alpha

Identifiers

PMID24351808
PMCPMC3876102
OpenAlexW1970035686

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.