Evidence map›Paper›PMID 27127934›Full record

ArticleInvestigative ophthalmology & visual science2016

Antioxidant Treatment Limits Neuroinflammation in Experimental Glaucoma.

Xiangjun Yang, Gözde Hondur, Gülgün Tezel

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

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  13. Protective Effects of Lipoxin AbioRxiv : the preprint server for biology · 2024
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1 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 2 countries.

Xiangjun Yang
Gözde Hondur
Gülgün Tezel
Columbia University · US

Funding

Instrumentation, Fabrication, and Design CoreP30EY019007 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Xin Zhang · 2010 to 2026
$12.9M
Oxidative Stress in Neurodegeneration & Neuroprotection in GlaucomaR21EY024105 · NEI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TEZEL, GULGUN · 2015 to 2016
$419k
NEI NIH HHS 1R21EY024105NEI NIH HHS P30 EY019007NEI NIH HHS R21 EY024105
6 · The paper itself

Abstract

purposeBesides primary neurotoxicity, oxidative stress may compromise the glial immune regulation and shift the immune homeostasis toward neurodegenerative inflammation in glaucoma. We tested this hypothesis through the analysis of neuroinflammatory and neurodegenerative outcomes in mouse glaucoma using two experimental paradigms of decreased or increased oxidative stress.

methodsThe first experimental paradigm tested the effects of Tempol, a multifunctional antioxidant, given through osmotic mini-pumps for drug delivery by constant infusion. Following a 6-week treatment period after microbead/viscoelastic injection-induced ocular hypertension, retina and optic nerve samples were analyzed for markers of oxidative stress and cytokine profiles using specific bioassays. We also analyzed a redox-sensitive transcriptional regulator of neuroinflammation, namely NF-κB. The second paradigm included a similar analysis of the effects of overloaded oxidative stress on retina and optic nerve inflammation in mice knockout for a major antioxidant enzyme (SOD1(-/-)).

resultsIncreased antioxidant capacity and decreased protein carbonyls and HNE adducts with Tempol treatment verified the drug delivery and biological function. Among a range of cytokines measured, proinflammatory cytokines, including IL-1, IL-2, IFN-γ, and TNF-α, exhibited more than 2-fold decreased titers in Tempol-treated ocular hypertensive eyes. Antioxidant treatment also resulted in a prominent decrease in NF-κB activation in the ocular hypertensive retina and optic nerve. Although pharmacological treatment limiting the oxidative stress resulted in decreased neuroinflammation, ocular hypertension-induced neuroinflammatory responses were increased in SOD1(-/-) mice with defective antioxidant response.

conclusionsThese findings support the oxidative stress-related mechanisms of neuroinflammation and the potential of antioxidant treatment as an immunomodulation strategy for neuroprotection in glaucoma.

Indexed as

AnimalsAntioxidantsBlotting, WesternCyclic N-OxidesCytokinesDisease Models, AnimalEnzyme-Linked Immunosorbent AssayGlaucomaInflammationInfusion Pumps, ImplantableIntraocular PressureMiceMice, Inbred C57BLNF-kappa BOcular HypertensionOptic NerveAntioxidantsCyclic N-OxidesCytokinesNF-kappa BSpin Labelstempol

Identifiers

PMID27127934
PMCPMC4855827
OpenAlexW2342445502

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.