Evidence map›Paper›PMID 38983569›Full record

ReviewFrontiers in ophthalmology2022

Molecular mechanisms of TGFβ-mediated EMT of retinal pigment epithelium in subretinal fibrosis of age-related macular degeneration.

Fumiaki Higashijima, Mina Hasegawa, Takuya Yoshimoto, Yuka Kobayashi, Makiko Wakuta, Kazuhiro Kimura

Abstract readReview
In one paragraph

Review in Frontiers in ophthalmology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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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

6 authors.

Fumiaki HigashijimaDepartment of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Mina HasegawaDepartment of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Takuya YoshimotoDepartment of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Yuka KobayashiDepartment of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Makiko WakutaDepartment of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
Kazuhiro KimuraDepartment of Ophthalmology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is one of the leading causes of blindness in the elderly, affecting the macula of the retina and resulting in vision loss. There are two types of AMD, wet and dry, both of which cause visual impairment. Wet AMD is called neovascular AMD (nAMD) and is characterized by the formation of choroidal neovascular vessels (CNVs) in the macula. nAMD can be treated with intravitreal injections of vascular endothelial growth factor (VEGF) inhibitors, which help improve vision. However, approximately half the patients do not achieve satisfactory results. Subretinal fibrosis often develops late in nAMD, leading to irreversible photoreceptor degeneration and contributing to visual loss. Currently, no treatment exists for subretinal fibrosis, and the molecular mechanisms of fibrous tissue formation following neovascular lesions remain unclear. In this review, we describe the clinical features and molecular mechanisms of macular fibrosis secondary to nAMD. Myofibroblasts play an essential role in the development of fibrosis. This review summarizes the latest findings on the clinical features and cellular and molecular mechanisms of the pathogenesis of subretinal fibrosis in nAMD and discusses the potential therapeutic strategies to control subretinal fibrosis in the future.

Indexed as

chronic inflammationepithelial-mesenchymal transformationmyofibroblastsubretinal fibrosisTGF-β

Identifiers

PMID38983569
PMCPMC11182173

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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.