Evidence map›Paper›PMID 24408972›Full record

ArticleInvestigative ophthalmology & visual science2014

TWEAK/Fn14 pathway is a novel mediator of retinal neovascularization.

Hossein Ameri, Hua Liu, Rong Liu, Yonju Ha, Adriana A Paulucci-Holthauzen, Shuqun Hu, Massoud Motamedi, Bernard F Godley, Ronald G Tilton, Wenbo Zhang

Open access · hybridAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  20. Survivin contributes to the progression of diabetic retinopathy through HIF-1α pathway.International journal of clinical and experimental pathology · 2015
    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

10 authors at 2 institutions in 2 countries.

Hossein AmeriDepartment of Ophthalmology and Visual Sciences, the University of Texas Medical Branch, Galveston, Texas.
Hua Liu
Rong Liu
Yonju Ha
Adriana A Paulucci-Holthauzen
Shuqun Hu
Massoud Motamedi
Bernard F Godley
Ronald G Tilton
Wenbo Zhang
The University of Texas Medical Branch at Galveston · USTongji Hospital · CN

Funding

Mechanisms of Retinal Neuronal InjuryR01EY022694 · NEI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ZHANG, WENBO · 2012 to 2021
$3.8M
NEI NIH HHS EY022694NEI NIH HHS R01 EY022694
6 · The paper itself

Abstract

purposeRetinal neovascularization (NV) is a major cause of vision loss in ischemia-induced retinopathy. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) and its receptor, fibroblast growth factor inducible-14 (Fn14), have been implicated in angiogenesis, but their role in retinal diseases is unknown. The goal of this study was to investigate the role of TWEAK/Fn14 pathway in retinal NV.

methodsStudies were performed in a mouse model of oxygen-induced retinopathy (OIR) and in primary human retinal microvascular endothelial cells (HRMECs). Hyperoxia treatment was initiated on postnatal day (P)14. Immunohistochemistry and quantitative PCR (qPCR) were used to assess retinal vascular changes in relation to expression of Fn14 and TWEAK.

resultsFibroblast growth factor-inducible 14 mRNA was prominently increased from P13 to P17 in OIR retinas, whereas TWEAK level was slightly decreased. These alterations were normalized by hyperoxia treatment and were more striking in isolated retinal vessels. There was a discernible shift in the immunoreactivity of Fn14 and TWEAK from the neuronal layers in the healthy retina to the neovascular tufts in that of OIR. Blockade of TWEAK/Fn14 significantly prevented retinal NV while slightly accelerated revascularization. In contrast, activation of Fn14 positively regulated survival pathways in the B-cell lymphoma-2 (Bcl2) family and robustly enhanced HRMEC survival. Furthermore, gene analysis revealed the regulatory region of Fn14 gene contains several conserved hypoxia inducible factor (HIF)-1α binding sites. Overexpression of HIF-1α prominently induced Fn14 expression in HRMECs.

conclusionsWe found that the TNF-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor inducible-14 (Fn14) pathway is involved in the development of pathologic retinal neovascularization. Hypoxia inducible factor-1α is likely implicated in the upregulation of Fn14.

Indexed as

AnimalsApoptosisBlotting, WesternCells, CulturedCytokine TWEAKDisease Models, AnimalEndothelial CellsFluorescent Antibody Technique, IndirectGene Expression RegulationHumansHypoxia-Inducible Factor 1, alpha SubunitMiceMice, Inbred C57BLReal-Time Polymerase Chain ReactionReceptors, Tumor Necrosis FactorRegulatory Sequences, Nucleic AcidCytokine TWEAKHIF1A protein, humanHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitReceptors, Tumor Necrosis FactorRNA, MessengerTNFRSF12A protein, humanTnfrsf12a protein, mouseTNFSF12 protein, humanTnfsf12 protein, mouseTumor Necrosis Factor InhibitorsTumor Necrosis FactorsTWEAK ReceptorFn14ischemia-induced retinopathyneovascularizationretinaTWEAK

Identifiers

PMID24408972
PMCPMC3920863
OpenAlexW2312946400

What OpenQuestion holds

Textmetadata
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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.