Evidence map›Paper›PMID 26505191›Full record

ArticlePloS one2015

Losartan Treatment Protects Retinal Ganglion Cells and Alters Scleral Remodeling in Experimental Glaucoma.

Harry A Quigley, Ian F Pitha, Derek S Welsbie, Cathy Nguyen, Matthew R Steinhart, Thao D Nguyen, Mary Ellen Pease, Ericka N Oglesby, Cynthia A Berlinicke, Katherine L Mitchell and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.8field-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

41 citing papers in PubMed, 62 citations in OpenAlex.

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  17. The Role of Axonal Transport in Glaucoma.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Decorin-An Antagonist of TGF-β in Astrocytes of the Optic Nerve.International journal of molecular sciences · 2021
    Article
  20. 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

13 authors at 2 institutions in 1 country.

Harry A QuigleyThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Ian F PithaThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Derek S WelsbieThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Cathy NguyenThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Matthew R SteinhartThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Thao D NguyenDepartment of Mechanical Engineering, Johns Hopkins University, Baltimore, Maryland, United States of America.
Mary Ellen PeaseThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Ericka N OglesbyThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Cynthia A BerlinickeThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Katherine L MitchellThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Jessica KimThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Joan J JefferysThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Elizabeth C KimballThe Glaucoma Center of Excellence, Wilmer Ophthalmological Institute, Johns Hopkins University, Baltimore, Maryland, United States of America.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Wilmer Core Grant for Vision ResearchP30EY001765 · NEI · JOHNS HOPKINS UNIVERSITY · PI Ji Yi · 1985 to 2026
$22.1M
PATHOGENESIS OF GLAUCOMATOUS OPTIC NERVE DAMAGER01EY002120 · NEI · JOHNS HOPKINS UNIVERSITY · PI QUIGLEY, HARRY ALAN · 1985 to 2025
$12.6M
Strategies to achieve sustained medication delivery in glaucoma treatmentK08EY024952 · NEI · JOHNS HOPKINS UNIVERSITY · PI PITHA, IAN FRANZ · 2015 to 2019
$957k
The Biomechanics of the Human Posterior Sclera: Effects of Age, Sex, and GlaucomaR01EY021500 · NEI · JOHNS HOPKINS UNIVERSITY · PI NGUYEN, THAO D · 2011 to 2016
$933k
Pathogenesis of Glaucomatous Optic Nerve DamageR56EY002120 · NEI · JOHNS HOPKINS UNIVERSITY · PI QUIGLEY, HARRY ALAN · 2008 to 2008
$369k
NEI NIH HHS EY01765NEI NIH HHS EY02120NEI NIH HHS K08 EY024952NEI NIH HHS P30 EY001765NEI NIH HHS R01 EY002120NEI NIH HHS R01 EY021500NEI NIH HHS R56 EY002120
6 · The paper itself

Abstract

purposeTo determine if oral losartan treatment decreases the retinal ganglion cell (RGC) death caused by experimental intraocular pressure (IOP) elevation in mice.

methodsWe produced IOP increase in CD1 mice and performed unilateral optic nerve crush. Mice received oral losartan, spironolactone, enalapril, or no drug to test effects of inhibiting angiotensin receptors. IOP was monitored by Tonolab, and blood pressure was monitored by tail cuff device. RGC loss was measured in masked axon counts and RGC bodies by β-tubulin labeling. Scleral changes that could modulate RGC injury were measured including axial length, scleral thickness, and retinal layer thicknesses, pressure-strain behavior in inflation testing, and study of angiotensin receptors and pathways by reverse transcription polymerase chain reaction, Western blot, and immunohistochemistry.

resultsLosartan treatment prevented significant RGC loss (median loss = 2.5%, p = 0.13), while median loss with water, spironolactone, and enalapril treatments were 26%, 28% and 43%; p < 0.0001). The lower RGC loss with losartan was significantly less than the loss with spironolactone or enalapril (regression model p = 0.001; drug treatment group term p = 0.01). Both losartan and enalapril significantly lowered blood pressure (p< 0.001), but losartan was protective, while enalapril led to worse than water-treated RGC loss. RGC loss after crush injury was unaffected by losartan treatment (difference from control p = 0.9). Survival of RGC in cell culture was not prolonged by sartan treatment. Axonal transport blockade after 3 day IOP elevations was less in losartan-treated than in control glaucoma eyes (p = 0.007). Losartan inhibited effects of glaucoma, including reduction in extracellular signal-related kinase activity and modification of glaucoma-related changes in scleral thickness and creep under controlled IOP.

conclusionsThe neuroprotective effect of losartan in mouse glaucoma is associated with adaptive changes in the sclera expressed at the optic nerve head.

Indexed as

AnimalsDisease Models, AnimalGlaucomaHumansIntraocular PressureLosartanMiceNeuroprotective AgentsOptic DiskRetinaRetinal Ganglion CellsScleraLosartanNeuroprotective Agents

Identifiers

PMID26505191
PMCPMC4624713
OpenAlexW1868721338

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.