Evidence map›Paper›PMID 34439904›Full record

ReviewBiomolecules2021

Targeting the NLRP3 Inflammasome in Glaucoma.

Sophie Coyle, Mohammed Naeem Khan, Melody Chemaly, Breedge Callaghan, Chelsey Doyle, Colin E Willoughby, Sarah D Atkinson, Meredith Gregory-Ksander, Victoria McGilligan

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
6.5field-weighted citation impact, top 2% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.

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  12. The P2X7 Receptor Regulates IL-1β Secretion in the Human Retina.International journal of molecular sciences · 2025
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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

9 authors at 3 institutions in 3 countries.

Sophie CoyleNorthern Ireland Centre for Stratified Medicine, Ulster University, Londonderry BT47 6SB, UK.
Mohammed Naeem KhanNorthern Ireland Centre for Stratified Medicine, Ulster University, Londonderry BT47 6SB, UK.
Melody ChemalyDepartment of Molecular Medicine and Surgery, Karolinska Institute, SE-171 76 Solna, Sweden.
Breedge CallaghanCentre for Molecular Biosciences, Biomedical Sciences Research Institute, Ulster University, Coleraine BT52 1SA, UK.
Chelsey DoyleCentre for Molecular Biosciences, Biomedical Sciences Research Institute, Ulster University, Coleraine BT52 1SA, UK.
Colin E WilloughbyCentre for Molecular Biosciences, Biomedical Sciences Research Institute, Ulster University, Coleraine BT52 1SA, UK.ORCID 0000-0002-1246-4166
Sarah D AtkinsonNorthern Ireland Centre for Stratified Medicine, Ulster University, Londonderry BT47 6SB, UK.
Meredith Gregory-KsanderDepartment of Ophthalmology, Schepens Eye Research Institute, Massachusetts Eye & Ear Infirmary and Harvard Medical School, Boston, MA 02114, USA.
Victoria McGilliganNorthern Ireland Centre for Stratified Medicine, Ulster University, Londonderry BT47 6SB, UK.
University of Ulster · GBKarolinska Institutet · SEMassachusetts Eye and Ear Infirmary · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glaucoma is a group of optic neuropathies characterised by the degeneration of retinal ganglion cells, resulting in damage to the optic nerve head (ONH) and loss of vision in one or both eyes. Increased intraocular pressure (IOP) is one of the major aetiological risk factors in glaucoma, and is currently the only modifiable risk factor. However, 30-40% of glaucoma patients do not present with elevated IOP and still proceed to lose vision. The pathophysiology of glaucoma is therefore not completely understood, and there is a need for the development of IOP-independent neuroprotective therapies to preserve vision. Neuroinflammation has been shown to play a key role in glaucoma and, specifically, the NLRP3 inflammasome, a key driver of inflammation, has recently been implicated. The NLRP3 inflammasome is expressed in the eye and its activation is reported in pre-clinical studies of glaucoma. Activation of the NLRP3 inflammasome results in IL-1β processing. This pro inflammatory cytokine is elevated in the blood of glaucoma patients and is believed to drive neurotoxic inflammation, resulting in axon degeneration and the death of retinal ganglion cells (RGCs). This review discusses glaucoma as an inflammatory disease and evaluates targeting the NLRP3 inflammasome as a therapeutic strategy. A hypothetical mechanism for the action of the NLRP3 inflammasome in glaucoma is presented.

Indexed as

AnimalsAnti-Inflammatory AgentsAxonsGlaucomaHumansInflammasomesInflammationInterleukin-1betaMiceNeuroprotectionNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesReceptors, Pattern RecognitionRetinal Ganglion CellsRisk FactorsAnti-Inflammatory AgentsIL1B protein, humanInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesReceptors, Pattern RecognitionglaucomainflammationNLRP3 inflammasomeRGC (retinal ganglion cells)

Identifiers

PMID34439904
PMCPMC8393362
OpenAlexW3194439524

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.