Evidence map›Paper›PMID 39586852›Full record

ArticleInternational ophthalmology2024

ANGPTL4 promotes choroidal neovascularization and subretinal fibrosis through the endothelial‒mesenchymal transition.

Jia Chen, Ying Yang, Shu Su, Shenglai Zhang, Ju Huang, Hong Chen, Xiaowei Yang, Aimin Sang

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In one paragraph

Article in International ophthalmology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Jia ChenSuzhou Medical College of Soochow University, Suzhou, 215123, China.
Ying YangEye Institute, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Shu SuSuzhou Medical College of Soochow University, Suzhou, 215123, China.
Shenglai ZhangEye Institute, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Ju HuangEye Institute, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Hong ChenEye Institute, Affiliated Hospital of Nantong University, Nantong, 226001, China.
Xiaowei YangEye Institute, Affiliated Hospital of Nantong University, Nantong, 226001, China. yangxiaowei0208@163.com.
Aimin SangSuzhou Medical College of Soochow University, Suzhou, 215123, China. sangam@ntu.edu.cn.

Funding

Postgraduate Research & Practice Innovation Program of Jiangsu Province KYCX21_3115Science and Technology Project of Nantong City MS12020031Science and Technology Project of Nantong City MSZ19035
6 · The paper itself

Abstract

purposeThis study aimed to investigate the possible mechanisms by which ANGPTL4 is involved in the pathogenesis of choroidal neovascularization (CNV) and subretinal fibrosis.

methodsDifferentially expressed genes in retinal pigmented epithelium (RPE)-choroid-sclera complex tissues from nAMD patients and control individuals were identified via the GEO database, followed by GO and KEGG analyses. A Venn diagram was used to identify EndMT-related DEGs. A logistic regression model was constructed to screen for prognostic genes. Laser-induced CNV mouse models were established and validated with FFA and OCTA. The expression of ANGPTL4 and EndMT-related markers in the RPE-choroid-sclera complex was measured via RT‒qPCR and Western blotting. TGF-β2-induced HUVECs were used as EndMT cell models, and specific siRNAs targeting ANGPTL4 (si-ANGPTL4) were designed and screened. The effects of ANGPTL4 knockdown on the migration and invasion of HUVECs were also examined. Laser-induced CNV mouse models were constructed, and an intravitreal injection of cholesterol-modified si-ANGPTL4 was used to knock down ANGPTL4. FFA, OCTA and immunofluorescence staining were used to observe CNV formation and subretinal fibrosis, and the expression of ANGPTL4 and EndMT-related markers was determined.

resultsANGPTL4 expression was significantly increased in mice with CNV and colocalized with IB4. In TGF-β2-induced EndMT, ANGPTL4 was also upregulated, and its knockdown led to the inhibition of EndMT and cell migration and invasion, while its overexpression promoted the EndMT process. ANGPTL4 knockdown reduced the formation of CNV and subretinal fibrosis in mice with CNV by suppressing EndMT.

conclusionsANGPTL4 may promote CNV and subretinal fibrosis through EndMT, suggesting that ANGPTL4 may be a novel potential target for nAMD therapy.

Indexed as

Angiopoietin-Like Protein 4Choroidal NeovascularizationDisease Models, AnimalEpithelial-Mesenchymal TransitionFibrosisMice, Inbred C57BLAnimalsCell MovementCells, CulturedChoroidEndothelial-Mesenchymal TransitionGene Expression RegulationHumansMaleMiceRetinal Pigment EpitheliumAngiopoietin-Like Protein 4ANGPTL4 protein, humanANGPTL4Choroidal neovascularizationEndothelial‒mesenchymal transitionSubretinal fibrosis

Identifiers

PMID39586852

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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.