Evidence map›Paper›PMID 32693061›Full record

ArticleThe American journal of pathology2020

Glaucoma after Ocular Surgery or Trauma: The Role of Infiltrating Monocytes and Their Response to Cytokine Inhibitors.

Xiaoniao Chen, Fengyang Lei, Chengxin Zhou, James Chodosh, Liqiang Wang, Yifei Huang, Claes H Dohlman, Eleftherios I Paschalis

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2020. 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
3.2field-weighted citation impact, top 7% 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. Intrinsic Optical Properties of Boston Keratoprosthesis.Translational vision science & technology · 2020
    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

8 authors at 2 institutions in 2 countries.

Xiaoniao ChenBoston Keratoprosthesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts; Department of Ophthalmology, Chinese PLA General Hospital, Beijing, China.
Fengyang LeiBoston Keratoprosthesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts.
Chengxin ZhouBoston Keratoprosthesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts.
James ChodoshBoston Keratoprosthesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts.
Liqiang WangDepartment of Ophthalmology, Chinese PLA General Hospital, Beijing, China.
Yifei HuangDepartment of Ophthalmology, Chinese PLA General Hospital, Beijing, China.
Claes H DohlmanBoston Keratoprosthesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts. Electronic address: claes_dohlman@meei.harvard.edu.
Eleftherios I PaschalisBoston Keratoprosthesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts. Electronic address: eleftherios_paschalis@meei.harvard.edu.
Massachusetts Eye and Ear Infirmary · USChinese PLA General Hospital · CN

Funding

VISION RESEARCHP30EY003790 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI Patricia Ann D'Amore · 1985 to 2026
$25.5M
Management of Blepharoptosis with Neodymium Magnet Systems: The Boston Blink-netic ProjectR01EY029437 · NEI · MASSACHUSETTS EYE AND EAR INFIRMARY · PI HOUSTON, KEVIN EDWARD · 2018 to 2022
$2.5M
NEI NIH HHS P30 EY003790NEI NIH HHS R01 EY029437
6 · The paper itself

Abstract

Glaucoma is a frequent and devastating long-term complication following ocular trauma, including corneal surgery, open globe injury, chemical burn, and infection. Postevent inflammation and neuroglial remodeling play a key role in subsequent ganglion cell apoptosis and glaucoma. To this end, this study was designed to investigate the amplifying role of monocyte infiltration into the retina. By using three different ocular injury mouse models (corneal suture, penetrating keratoplasty, and globe injury) and monocyte fate mapping techniques, we show that ocular trauma or surgery can cause robust infiltration of bone marrow-derived monocytes into the retina and subsequent neuroinflammation by up-regulation of Tnf, Il1b, and Il6 mRNA within 24 hours. This is accompanied by ganglion cell apoptosis and neurodegeneration. Prompt inhibition of tumor necrosis factor-α or IL-1β markedly suppresses monocyte infiltration and ganglion cell loss. Thus, acute ocular injury (surgical or trauma) can lead to rapid neuroretinal inflammation and subsequent ganglion cell loss, the hallmark of glaucoma. Infiltrating monocytes play a central role in this process, likely amplifying the inflammatory cascade, aiding in the activation of retinal microglia. Prompt administration of cytokine inhibitors after ocular injury prevents this infiltration and ameliorates the damage to the retina-suggesting that it may be used prophylactically for neuroprotection against post-traumatic glaucoma.

Indexed as

AnimalsBurns, ChemicalCorneaCytokinesDisease Models, AnimalGlaucomaMice, TransgenicMonocytesNeurogliaRetinaCytokines

Identifiers

PMID32693061
PMCPMC7527856
OpenAlexW3043523725

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.