Evidence map›Paper›PMID 37596693›Full record

ArticleJournal of translational medicine2023

Targeting FSCN1 with an oral small-molecule inhibitor for treating ocular neovascularization.

Wen Bai, Jun-Song Ren, Min Xia, Ya Zhao, Jing-Juan Ding, Xi Chen, Qin Jiang

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

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  11. Role of actin-binding proteins in prostate cancer.Frontiers in cell and developmental biology · 2024
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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 2 institutions in 1 country.

Wen Bai *The Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China.
Jun-Song Ren *The Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China.
Min Xia *The Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China.
Ya ZhaoThe Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China.
Jing-Juan DingThe Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China.
Xi ChenThe Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China.
Qin JiangThe Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China. jqin710@vip.sina.com.ORCID http://orcid.org/0000-0001-9154-8917
Second Affiliated Hospital of Nanjing Medical University · CNNorthern Jiangsu People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOcular neovascularization is a leading cause of blindness and visual impairment. While intravitreal anti-VEGF agents can be effective, they do have several drawbacks, such as endophthalmitis and drug resistance. Additional studies are necessary to explore alternative therapeutic targets.

methodsBioinformatics analysis and quantitative RT-PCR were used to detect and verify the FSCN1 expression levels in oxygen-induced retinopathy (OIR) and laser-induced choroidal neovascularization (CNV) mice model. Transwell, wound scratching, tube formation, three-dimensional bead sprouting assay, rhodamine-phalloidin staining, Isolectin B4 staining and immunofluorescent staining were conducted to detect the role of FSCN1 and its oral inhibitor NP-G2-044 in vivo and vitro. HPLC-MS/MS analysis, cell apoptosis assay, MTT assay, H&E and tunnel staining, visual electrophysiology testing, visual cliff test and light/dark transition test were conducted to assess the pharmacokinetic and security of NP-G2-044 in vivo and vitro. Co-Immunoprecipitation, qRT-PCR and western blot were conducted to reveal the mechanism of FSCN1 and NP-G2-044 mediated pathological ocular neovascularization.

resultsWe discovered that Fascin homologue 1 (FSCN1) is vital for angiogenesis both in vitro and in vivo, and that it is highly expressed in oxygen-induced retinopathy (OIR) and laser-induced choroidal neovascularization (CNV). We found that NP-G2-044, a small-molecule inhibitor of FSCN1 with oral activity, can impede the sprouting, migration, and filopodia formation of cultured endothelial cells. Oral NP-G2-044 can effectively and safely curb the development of OIR and CNV, and increase efficacy while overcoming anti-VEGF resistance in combination with intravitreal aflibercept (Eylea) injection.

conclusionCollectively, FSCN1 inhibition could serve as a promising therapeutic approach to block ocular neovascularization.

Indexed as

Choroidal NeovascularizationRetinal DiseasesAnimalsApoptosisCarrier ProteinsEndothelial CellsFuransIndazolesMiceMicrofilament ProteinsTandem Mass SpectrometryCarrier ProteinsFSCN1 protein, humanFuransIndazolesMicrofilament ProteinsNP-G2-044AngiogenesisFSCN1NP-G2-044Ocular pathologiesVascular tip cell

Identifiers

PMID37596693
PMCPMC10436462
OpenAlexW4385986442

What OpenQuestion holds

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LicenceCC BY
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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.