Evidence map›Paper›PMID 32993110›Full record

ArticleMolecules (Basel, Switzerland)2020

AR12286 Alleviates TGF-β-Related Myofibroblast Transdifferentiation and Reduces Fibrosis after Glaucoma Filtration Surgery.

Wen-Sheng Cheng, Ching-Long Chen, Jiann-Torng Chen, Le-Tien Lin, Shu-I Pao, Yi-Hao Chen, Da-Wen Lu

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

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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 3 institutions in 1 country.

Wen-Sheng ChengGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei 114, Taiwan.
Ching-Long ChenDepartment of Ophthalmology, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan.
Jiann-Torng ChenDepartment of Ophthalmology, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan.
Le-Tien LinDepartment of Ophthalmology, Tri-Service General Hospital Songshan Branch, National Defense Medical Center, Taipei 114, Taiwan.
Shu-I PaoDepartment of Ophthalmology, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan.
Yi-Hao ChenDepartment of Ophthalmology, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan.
Da-Wen LuGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei 114, Taiwan.
National Defense Medical Center · TWTri-Service General Hospital · TWTri-Service General Hospital Songshan Branch · TW

Funding

Tri-Service General Hospital, Taipei, Taiwan TSGH-E-109123
6 · The paper itself

Abstract

Scar formation can cause the failure of glaucoma filtration surgery. We investigated the effect of AR12286, a selective Rho-associated kinase inhibitor, on myofibroblast transdifferentiation and intraocular pressure assessment in rabbit glaucoma filtration surgery models. Cell migration and collagen contraction were used to demonstrate the functionality of AR12286-modulated human conjunctival fibroblasts (HConFs). Polymerase chain reaction quantitative analysis was used to determine the effect of AR12286 on the production of collagen Type 1A1 and fibronectin 1. Cell migration and collagen contraction in HConFs were activated by TGF-β1. However, compared with the control group, rabbit models treated with AR12286 exhibited higher reduction in intraocular pressure after filtration surgery, and decreased collagen levels at the wound site in vivo. Therefore, increased α-SMA expression in HConFs induced by TGF-β1 could be inhibited by AR12286, and the production of Type 1A1 collagen and fibronectin 1 in TGF-β1-treated HConFs was inhibited by AR12286. Overall, the stimulation of HConFs by TGF-β1 was alleviated by AR12286, and this effect was mediated by the downregulation of TGF-β receptor-related SMAD signaling pathways. In vivo results indicated that AR12286 thus improves the outcome of filtration surgery as a result of its antifibrotic action in the bleb tissue because AR12286 inhibited the TGF-β receptor-related signaling pathway, suppressing several downstream reactions in myofibroblast transdifferentiation.

Indexed as

Filtering SurgeryGlaucomaAnimalsCell LineCell TransdifferentiationFibrosisHumansMyofibroblastsProtein Kinase InhibitorsRabbitsSignal TransductionTransforming Growth Factor betaProtein Kinase InhibitorsTransforming Growth Factor betaAR12286glaucoma filtration surgeryhuman conjunctival fibroblastSMADTGF-βα-SMA

Identifiers

PMID32993110
PMCPMC7583051
OpenAlexW3087910349

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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.