Evidence map›Paper›PMID 39189995›Full record

ArticleInvestigative ophthalmology & visual science2024

The Necroptosis Pathway Is Upregulated in the Cornea in Mice With Ocular Graft-Versus-Host Disease.

Kazuki Asai, Hyung Keun Lee, Shinri Sato, Eisuke Shimizu, Jaehun Jung, Takahiro Okazaki, Mamoru Ogawa, Shigeto Shimmura, Kazuo Tsubota, Yoko Ogawa and 2 more

Abstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
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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

12 authors.

Kazuki AsaiDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Hyung Keun LeeOphthalmology, Yonsei University College of Medicine, Seoul, South Korea.
Shinri SatoDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Eisuke ShimizuDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Jaehun JungOphthalmology, Yonsei University College of Medicine, Seoul, South Korea.
Takahiro OkazakiDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Mamoru OgawaDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Shigeto ShimmuraDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Kazuo TsubotaDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Yoko OgawaDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Kazuno NegishiDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
Masatoshi HirayamaDepartment of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: To identify molecular signatures specific for ocular graft-versus-host disease (GVHD) by proteomic analysis of corneas from mice with GVHD. Methods: We identified differentially expressed proteins (DEPs) in corneal samples from GVHD model mice and syngeneic control mice 4 weeks after bone marrow transplantation. Data-independent acquisition analysis was performed on individual samples, and the roles of DEPs in biological pathways related to GVHD were evaluated via bioinformatics and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Results: Three important signaling pathways were upregulated in the cornea in mice with GVHD: (1) the necroptosis pathway, (2) the mitogen-activated protein kinase (MAPK) pathway, and (3) as previously reported, the neutrophil extracellular trap (NET) pathway. In those signaling pathways, we identified new upregulated molecules, including (1) receptor-interacting protein kinase 1 (RIPK1), RIPK3, interferon regulatory factor 9, the interferon-induced double-stranded RNA-activated protein kinase lipoxygenase, and high mobility group box1 (HMGB1) which are damage-associated molecular patterns (DAMPs) in the necroptosis pathway; (2) the sequentially upregulated interleukin 1 (IL-1) receptor-associated kinase (IRAK), an evolutionarily conserved signaling intermediate in the Toll pathway (ECSIT), and p38, which is downstream of the IL-1 receptor and increased CDC42/Rac (Rac2), a Rho family GTPase in the MAPK pathway; and (3) the integrin components CR3 and macrophage-1 antigen (MAC-1), which are DAMPs, and the pyroptosis-related protein gasdermin D (GSDMD) in the NET pathway. Conclusions: These novel molecules may help researchers elucidate the pathogenesis of GVHD and identify new therapeutic targets for corneal changes in patients with ocular GVHD.

Indexed as

CorneaDisease Models, AnimalGraft vs Host DiseaseMice, Inbred C57BLNecroptosisProteomicsSignal TransductionUp-RegulationAnimalsBone Marrow TransplantationFemaleMice

Identifiers

PMID39189995
PMCPMC11361379

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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.