Evidence map›Paper›PMID 34440742›Full record

ReviewCells2021

Immune Responses in the Glaucomatous Retina: Regulation and Dynamics.

Valery I Shestopalov, Markus Spurlock, Oliver W Gramlich, Markus H Kuehn

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
10.3field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  4. Microglial polarization in retinal neovascularization: Friend or foe?Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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  19. Generation of xenobiotic free retinofugal assembloids.Frontiers in cell and developmental biology · 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

4 authors at 3 institutions in 2 countries.

Valery I ShestopalovDepartment of Ophthalmology, Miller School of Medicine, University of Miami, Miami, FL 33101, USA.
Markus SpurlockDepartment of Cell and Developmental Biology, Miller School of Medicine, University of Miami, Miami, FL 33101, USA.
Oliver W GramlichDepartment of Veterans Affairs, Center for the Prevention and Treatment of Visual Loss, Iowa City, IA 52246, USA.
Markus H KuehnDepartment of Veterans Affairs, Center for the Prevention and Treatment of Visual Loss, Iowa City, IA 52246, USA.
University of Iowa · USInstitute for Information Transmission Problems · RUUniversity of Miami · US

Funding

The Role of Pannexin 1 Pathway in Ocular Hypertension Injury of Retinal Ganglion CellsR01EY021517 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SHESTOPALOV, VALERY I · 2012 to 2020
$3.1M
T-cell mediated RGC damage in glaucoma Diversity Initiative SupplementR01EY034534 · NEI · UNIVERSITY OF IOWA · PI MARKUS H. KUEHN · 2023 to 2026
$2.5M
Role of gasderminD in ganglion cell dysfunction and injuryR21EY032261 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SHESTOPALOV, VALERY I · 2021 to 2022
$407k
Role and regulation of inflammasome in the intraocular pressure-induced injury of retinal ganglion cellsF31EY032789 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SPURLOCK, MARKUS · 2022 to 2024
$143k
Center for the Prevention and Treatment of Visual LossI50RX003002 · VA · IOWA CITY VA MEDICAL CENTER · PI RANDY H. KARDON, MARKUS H. KUEHN · 2019 to 2026
–
NEI NIH HHS F31 EY032789NEI NIH HHS R01 EY021517NEI NIH HHS R01 EY034534NEI NIH HHS R21 EY032261NIH HHS EY032261Rehabilitation Research and Development Service I01 RX002860-01RRD VA I01 RX002860U.S. Department of Defense VR200079
6 · The paper itself

Abstract

Glaucoma is a multifactorial disease resulting in progressive vision loss due to retinal ganglion cell (RGC) dysfunction and death. Early events in the pathobiology of the disease include oxidative, metabolic, or mechanical stress that acts upon RGC, causing these to rapidly release danger signals, including extracellular ATP, resulting in micro- and macroglial activation and neuroinflammation. Danger signaling also leads to the formation of inflammasomes in the retina that enable maturation of proinflammatory cytokines such IL-1β and IL-18. Chronic neuroinflammation can have directly damaging effects on RGC, but it also creates a proinflammatory environment and compromises the immune privilege of the retina. In particular, continuous synthesis of proinflammatory mediators such as TNFα, IL-1β, and anaphylatoxins weakens the blood-retina barrier and recruits or activates T-cells. Recent data have demonstrated that adaptive immune responses strongly exacerbate RGC loss in animal models of the disease as T-cells appear to target heat shock proteins displayed on the surface of stressed RGC to cause their apoptotic death. It is possible that dysregulation of these immune responses contributes to the continued loss of RGC in some patients.

Indexed as

Adenosine TriphosphateCytokinesGlaucomaHumansImmunity, InnateInflammasomesRetinal Ganglion CellsSignal TransductionAdenosine TriphosphateCytokinesInflammasomesadaptive immune responsedysfunctionglaucomainflammasomeinnate immune response

Identifiers

PMID34440742
PMCPMC8391899
OpenAlexW3187363453

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.