Evidence map›Paper›PMID 40556366›Full record

ArticleGenes to cells : devoted to molecular & cellular mechanisms2025

Effects of Dual Inhibition of VEGF-A and Angpt-2 on Angiogenesis and Lymphangiogenesis in an Alkali-Induced Corneal Injury Model.

Hiroshi Kuribayashi, Toshiro Iwagawa, Souta Kadohara, Hirokazu Ohashi, Chihiro Kawaji, Takeru Iida, Tomoya Suzuki, Yuta Inokuchi, Tetsuhiro Soeda, Kosuke Saita and 4 more

Abstract read
In one paragraph

Article in Genes to cells : devoted to molecular & cellular mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

14 authors.

Hiroshi KuribayashiDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Toshiro IwagawaDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0003-1600-7795
Souta KadoharaDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Hirokazu OhashiDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Chihiro KawajiDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Takeru IidaDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Tomoya SuzukiDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yuta InokuchiDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0009-0004-2385-3505
Tetsuhiro SoedaProduct Research Department, Chugai Pharmaceutical Co., Ltd., Tokyo, Japan.
Kosuke SaitaDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Makoto AiharaDepartment of Ophthalmology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Nobuyuki EbiharaDepartment of Ophthalmology, Juntendo University Urayasu Hospital, Chiba, Japan.
Takashi MiyaiDepartment of Ophthalmology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0001-5286-8272
Sumiko WatanabeDepartment of Retinal Biology and Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0003-4497-5750

Funding

Chugai Pharmaceutical
6 · The paper itself

Abstract

Corneal neovascularization (CNV) is frequently observed after various corneal injuries and corneal transplantation, leading to impairment of corneal transparency. Lymphangiogenesis and the inflammatory response often accompany CNV. Chemical injury is one of the most common causes of CNV, and alkali injury has been widely used as an animal model of this pathological state. We examined the effects of subconjunctival injection of an anti-VEGFA antibody (anti-VEGFA_ab), anti-ANGPT2 antibody (anti-ANGPT2_ab), and bispecific antibody against VEGFA and ANGPT2 (BsAb) in CNV using the alkali injury mouse model. The pathological indexes were examined using anterior segment optical coherence tomography (OCT) and whole-mount immunostaining, and gene expression patterns were examined using RT-qPCR. Treatment with anti-VEGFA_ab, anti-ANGPT2_ab, or BsAb did not affect the swelled thickness of the cornea; however, angiogenesis, but not lymphangiogenesis, was hampered by the treatment of either one of the antibodies. We observed an increase in the mRNA levels of Vegfa, Angpt2, Il1b, and Cx3cr1 following alkali injury. The administration of BsAb suppressed the induction of Vegfa and Cx3cr1. Additionally, BsAb treatment enhanced the mRNA levels of Angpt1 in this model. This study demonstrates the potential of dual VEGFA and ANGPT2 inhibition as a therapeutic strategy for CNV.

Indexed as

Angiopoietin-2Corneal InjuriesCorneal NeovascularizationLymphangiogenesisVascular Endothelial Growth Factor AAlkaliesAngiogenesisAnimalsCorneaDisease Models, AnimalMaleMiceMice, Inbred C57BLAlkaliesAngiopoietin-2Angpt2 protein, mouseVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseangiogenesisANGPT2cornealymphangiogenesisVEGFA

Identifiers

PMID40556366
PMCPMC12188107

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Registered trials

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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.