Evidence map›Paper›PMID 30373222›Full record

ReviewInternational journal of molecular sciences2018

Reactive Oxygen Species-Mediated Damage of Retinal Neurons: Drug Development Targets for Therapies of Chronic Neurodegeneration of the Retina.

Landon J Rohowetz, Jacob G Kraus, Peter Koulen

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed.

  1. Review
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  4. Biomechanical Modification of the Sclera: An Ex Vivo Study on Porcine Eyes.Investigative ophthalmology & visual science · 2026
    Article
  5. Article
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  7. Review
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  9. Diabetic retinopathy and Alzheimer's disease: Convergence of the unfolded protein response in neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
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  11. 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

3 authors.

Landon J RohowetzVision Research Center, Department of Ophthalmology, School of Medicine, University of Missouri-Kansas City, 2411 Holmes St., Kansas City, MO 64108, USA. ljrvx8@mail.umkc.edu.ORCID 0000-0002-5403-421X
Jacob G KrausVision Research Center, Department of Ophthalmology, School of Medicine, University of Missouri-Kansas City, 2411 Holmes St., Kansas City, MO 64108, USA. jgkppb@umkc.edu.
Peter KoulenVision Research Center, Department of Ophthalmology, School of Medicine, University of Missouri-Kansas City, 2411 Holmes St., Kansas City, MO 64108, USA. koulenp@umkc.edu.

Funding

A Novel Neuroprotective Approach for GlaucomaR01EY027005 · NEI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI KATALIN T PROKAI · 2016 to 2026
$3.9M
Novel mechanism of action as therapeutic strategy for optic neuritisR01EY022774 · NEI · UNIVERSITY OF MISSOURI KANSAS CITY · PI KOULEN, PETER · 2012 to 2014
$1.2M
National Eye Institute EY022774National Eye Institute EY027005Research to Prevent Blindness Challenge Grant
6 · The paper itself

Abstract

The significance of oxidative stress in the development of chronic neurodegenerative diseases of the retina has become increasingly apparent in recent years. Reactive oxygen species (ROS) are free radicals produced at low levels as a result of normal cellular metabolism that are ultimately metabolized and detoxified by endogenous and exogenous mechanisms. In the presence of oxidative cellular stress, ROS are produced in excess, resulting in cellular injury and death and ultimately leading to tissue and organ dysfunction. Recent studies have investigated the role of excess ROS in the pathogenesis and development of chronic neurodegenerative diseases of the retina including glaucoma, diabetic retinopathy, and age-related macular degeneration. Findings from these studies are promising insofar as they provide clear rationales for innovative treatment and prevention strategies of these prevalent and disabling diseases where currently therapeutic options are limited. Here, we briefly outline recent developments that have contributed to our understanding of the role of ROS in the pathogenesis of chronic neurodegenerative diseases of the retina. We then examine and analyze the peer-reviewed evidence in support of ROS as targets for therapy development in the area of chronic neurodegeneration of the retina.

Indexed as

AnimalsAntioxidantsDrug DevelopmentHumansNeuroprotective AgentsReactive Oxygen SpeciesRetinal DegenerationRetinal NeuronsAntioxidantsNeuroprotective AgentsReactive Oxygen Speciesage-related macular degenerationbiologicalsdiabetic retinopathyglaucomaoxidative stressreactive oxygen speciesretinasmall moleculestherapy

Identifiers

PMID30373222
PMCPMC6274960

What OpenQuestion holds

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LicenceCC BY
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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.