Evidence map›Paper›PMID 28406452›Full record

ArticleToxins2017

Suppression of Hepatic Epithelial-to-Mesenchymal Transition by Melittin via Blocking of TGFβ/Smad and MAPK-JNK Signaling Pathways.

Ji-Hyun Park, Byoungduck Park, Kwan-Kyu Park

Open access · goldAbstract read
In one paragraph

Article in Toxins, 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
3.6field-weighted citation impact, top 7% 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, 34 citations in OpenAlex.

  1. Melittin attenuates imiquimod-induced psoriatic dermatitis in mice: a role for autophagy activation via PI3K/Akt/mTOR pathway suppression.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Melittin alleviates bleomycin-induced pulmonary fibrosisIranian journal of basic medical sciences · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. BHLHE41 suppresses MCF-7 cell invasion via MAPK/JNK pathway.Journal of cellular and molecular medicine · 2020
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. [Tumor necrosis factor-α and transforming growth factor-βNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    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

3 authors at 2 institutions in 1 country.

Ji-Hyun ParkCollege of Pharmacy, Keimyung University, Dalgubeoldaero, Dalseo-Gu, Daegu 42601, Korea. jihyunp@kmu.ac.kr.
Byoungduck ParkCollege of Pharmacy, Keimyung University, Dalgubeoldaero, Dalseo-Gu, Daegu 42601, Korea. bdpark@kmu.ac.kr.
Kwan-Kyu ParkDepartment of Pathology, Daegu Catholic University Medical Center, Duryugongwon-ro, Nam-gu, Daegu 42472, Korea. kkpark@cu.ac.kr.
Keimyung University · KRDaegu Catholic University Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor (TGF)-β1 plays a crucial role in the epithelial-to-mesenchymal transition (EMT) in hepatocytes and hepatic stellate cells (HSC), which contributes to the pathogenesis of liver fibrosis. Melittin (MEL) is a major component of bee venom and is effective in rheumatoid arthritis, pain relief, cancer cell proliferation, fibrosis and immune modulating activity. In this study, we found that MEL inhibits hepatic EMT in vitro and in vivo, regulating the TGFβ/Smad and TGFβ/nonSmad signaling pathways. MEL significantly inhibited TGF-β1-induced expression of EMT markers (E-cadherin reduction and vimentin induction) in vitro. These results were confirmed in CCl₄-induced liver in vivo. Treatment with MEL almost completely blocked the phosphorylation of Smad2/3, translocation of Smad4 and phosphorylation of JNK in vitro and in vivo. Taken together, these results suggest that MEL suppresses EMT by inhibiting the TGFβ/Smad and TGFβ/nonSmad-c-Jun N-terminal kinase (JNK)/Mitogen-activated protein kinase (MAPK) signaling pathways. These results indicated that MEL possesses potent anti-fibrotic and anti-EMT properties, which may be responsible for its effects on liver diseases.

Indexed as

AnimalsCarbon TetrachlorideCell LineChemical and Drug Induced Liver InjuryEpithelial-Mesenchymal TransitionHepatic Stellate CellsHepatocytesJNK Mitogen-Activated Protein KinasesLiver CirrhosisMaleMelittenMice, Inbred C57BLRatsSmad ProteinsTransforming Growth Factor beta1Carbon TetrachlorideJNK Mitogen-Activated Protein KinasesMelittenSmad ProteinsTransforming Growth Factor beta1epithelial-to-mesenchymal transitionliver diseasesmelittintransforming growth factor

Identifiers

PMID28406452
PMCPMC5408212
OpenAlexW2606666785

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.