Evidence map›Paper›PMID 37298577›Full record

ArticleInternational journal of molecular sciences2023

High VEGF Concentrations Accelerate Human Trabecular Meshwork Fibrosis in a TAZ-Dependent Manner.

Mi Sun Sung, So Young Kim, Gwang Hyeon Eom, Sang Woo Park

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Mechanobiology in the eye.npj biological physics and mechanics · 2025
    Review
  5. Article
  6. Review
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

4 authors at 2 institutions in 1 country.

Mi Sun SungDepartment of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Republic of Korea.ORCID 0000-0001-7512-7303
So Young KimDepartment of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Republic of Korea.
Gwang Hyeon EomDepartment of Pharmacology, Chonnam National University Medical School, Hwasun 58128, Republic of Korea.
Sang Woo ParkDepartment of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Republic of Korea.
Chonnam National University Hospital · KRChonnam National University Hwasun Hospital · KR

Funding

2020 Cheil-Nammyung Foundation Research Fund 2020 Cheil-Nammyung Foundation Research FundChonnam National University Hospital Biomedical Research Institute BCRI20026, BCRI23078National Research Foundation of Korea 2021R1G1A1094463
6 · The paper itself

Abstract

We aimed to investigate the effects of different concentrations of vascular endothelial growth factor (VEGF) on the extracellular matrix (ECM) and fibrotic proteins in human trabecular meshwork (TM) cells. We also explored how the Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ) signaling pathway modulates VEGF-induced fibrosis. We determined cross-linked actin network (CLAN) formation using TM cells. Changes in fibrotic and ECM protein expression were determined. High VEGF concentrations (10 and 30 ng/mL) increased TAZ and decreased p-TAZ/TAZ expression in TM cells. Western blotting and real-time PCR revealed no YAP expression changes. Fibrotic and ECM protein expression decreased at low VEGF concentrations (1 and 10 ρg/mL) and significantly increased at high VEGF concentrations (10 and 30 ng/mL). CLAN formation increased in TM cells treated with high VEGF concentrations. Moreover, TAZ inhibition by verteporfin (1 μM) rescued TM cells from high-VEGF-concentration-induced fibrosis. Low VEGF concentrations reduced fibrotic changes, whereas high VEGF concentrations accelerated fibrosis and CLAN formations in TM cells in a TAZ-dependent manner. These findings reflect the dose-dependent influences of VEGF on TM cells. Moreover, TAZ inhibition might be a therapeutic target for VEGF-induced TM dysfunction.

Indexed as

Adaptor Proteins, Signal TransducingTrabecular MeshworkVascular Endothelial Growth Factor AActinsCells, CulturedExtracellular Matrix ProteinsFibrosisHumansIntracellular Signaling Peptides and ProteinsTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsYAP-Signaling ProteinsActinsAdaptor Proteins, Signal TransducingExtracellular Matrix ProteinsIntracellular Signaling Peptides and ProteinsTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsVascular Endothelial Growth Factor AYAP-Signaling Proteinsfibrosishuman trabecular meshworkTAZVEGF

Identifiers

PMID37298577
PMCPMC10253844
OpenAlexW4379230465

What OpenQuestion holds

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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.