Evidence map›Paper›PMID 30483803›Full record

ArticleMolecular medicine reports2019

MEK inhibition prevents TGF‑β1‑induced myofibroblast transdifferentiation in human tenon fibroblasts.

Jiamin Wen, Xianchai Lin, Wuyou Gao, Bo Qu, Yunlan Ling, Rongjiao Liu, Minbin Yu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Involvement of METTL3/mJournal of molecular histology · 2021
    Article
  8. Article
  9. Cooperative signaling between integrins and growth factor receptors in fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  10. Article
  11. 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 1 institution in 1 country.

Jiamin Wen *State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Xianchai Lin *State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Wuyou GaoState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Bo QuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Yunlan LingState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Rongjiao LiuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Minbin YuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subconjunctival fibrosis represents the primary cause of postoperative failure of trabeculectomy, and at present there is a lack of effective intervention strategies. The present study aimed to investigate the effect of the mitogen‑activated protein kinase kinase (MEK) inhibitor U0126 on human tenon fibroblast (HTF) myofibrosis transdifferentiation, and to illuminate the underlying molecular mechanisms involved. It was demonstrated that U0126 significantly inhibited the proliferation, migration and collagen contraction of HTFs stimulated with TGF‑β1. In addition, U0126 largely attenuated the TGF‑β1‑induced conversion of HTFs into myofibroblasts, as indicated by a downregulation of the mRNA and protein expression of α‑smooth muscle actin and zinc finger protein SNAI1, and by ameliorating the 3D‑collagen contraction response. Mechanistically, U0126 suppressed the TGF‑β1‑stimulated phosphorylation of mothers against decapentaplegic homolog 2/3, P38 mitogen‑activated protein kinase and extracellular signal‑regulated kinase 1/2, indicating that U0126 may inhibit HTF activation through the canonical and non‑canonical signaling pathways of TGF‑β1. Therefore, U0126 exhibits a potent anti‑fibrotic effect among HTFs, and the inhibition of MEK signaling may serve as an alternative intervention strategy for the treatment of trabeculectomy‑associated fibrosis.

Indexed as

ActinsButadienesCell DifferentiationCell MovementCell ProliferationCells, CulturedCell TransdifferentiationCollagenDown-RegulationFibroblastsFibrosisHumansMitogen-Activated Protein KinasesMyofibroblastsNitrilesPhosphorylationActinsButadienesCollagenMitogen-Activated Protein KinasesNitrilesRNA, MessengerSnail Family Transcription FactorsTGFB1 protein, humanTransforming Growth Factor beta1U 0126glaucoma filtration surgeryhuman tenon fibroblastsmitogen-activated protein kinase kinase inhibitorsubconjunctival fibrosistransforming growth factor-β1

Identifiers

PMID30483803
PMCPMC6297771
OpenAlexW2900728110

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.