Evidence map›Paper›PMID 28807717›Full record

ReviewProgress in retinal and eye research2017

Myofibroblast transdifferentiation: The dark force in ocular wound healing and fibrosis.

Daisy Y Shu, Frank J Lovicu

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Progress in retinal and eye research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
219citing papers in PubMed, 2 pooled it
16.7field-weighted citation impact, top 1% 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

219 citing papers in PubMed, 2 syntheses or guidelines pooled it, 366 citations in OpenAlex.

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  11. ALKBH5 aggravates scarring after glaucoma surgery via mCell death and differentiation · 2026
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159 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Daisy Y ShuDiscipline of Anatomy and Histology, Bosch Institute, University of Sydney, NSW, Australia; Save Sight Institute, University of Sydney, NSW, Australia.
Frank J LovicuDiscipline of Anatomy and Histology, Bosch Institute, University of Sydney, NSW, Australia; Save Sight Institute, University of Sydney, NSW, Australia. Electronic address: frank.lovicu@sydney.edu.au.
The University of Sydney · AU

Funding

STUDIES ON LENS DIFFERENTIATION: ROLE OF FGFR01EY003177 · NEI · UNIVERSITY OF SYDNEY · PI LOVICU, FRANK JAMES, MCAVOY, JOHNSTON W · 1985 to 2015
$1.8M
NEI NIH HHS R01 EY003177
6 · The paper itself

Abstract

Wound healing is one of the most complex biological processes to occur in life. Repair of tissue following injury involves dynamic interactions between multiple cell types, growth factors, inflammatory mediators and components of the extracellular matrix (ECM). Aberrant and uncontrolled wound healing leads to a non-functional mass of fibrotic tissue. In the eye, fibrotic disease disrupts the normally transparent ocular tissues resulting in irreversible loss of vision. A common feature in fibrotic eye disease is the transdifferentiation of cells into myofibroblasts that can occur through a process known as epithelial-mesenchymal transition (EMT). Myofibroblasts rapidly produce excessive amounts of ECM and exert tractional forces across the ECM, resulting in the distortion of tissue architecture. Transforming growth factor-beta (TGFβ) plays a major role in myofibroblast transdifferentiation and has been implicated in numerous fibrotic eye diseases including corneal opacification, pterygium, anterior subcapsular cataract, posterior capsular opacification, proliferative vitreoretinopathy, fibrovascular membrane formation associated with proliferative diabetic retinopathy, submacular fibrosis, glaucoma and orbital fibrosis. This review serves to introduce the pathological functions of the myofibroblast in fibrotic eye disease. We also highlight recent developments in elucidating the multiple signaling pathways involved in fibrogenesis that may be exploited in the development of novel anti-fibrotic therapies to reduce ocular morbidity due to scarring.

Indexed as

Cell TransdifferentiationEpithelial-Mesenchymal TransitionEye DiseasesFibrosisHumansMyofibroblastsSignal TransductionTransforming Growth Factor betaWound HealingTransforming Growth Factor betaEpithelial-mesenchymal transition (EMT)FibrosisMyofibroblastOcularTransforming growth factor-beta (TGFβ)Wound healing

Identifiers

PMID28807717
PMCPMC5600870
OpenAlexW2742591033

What OpenQuestion holds

Textmetadata
LicenceTDM
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.