Evidence map›Paper›PMID 23821198›Full record

ArticleInvestigative ophthalmology & visual science2013

SIRT1 promotes RGC survival and delays loss of function following optic nerve crush.

Ling Zuo, Reas S Khan, Vivian Lee, Kimberly Dine, Wen Wu, Kenneth S Shindler

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Update on Nicotinamide and Its Application in the Management of Glaucoma.International journal of molecular sciences · 2025
    Review
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  14. Cell-Specific Expression of Human SIRT1 by Gene Therapy Reduces Retinal Ganglion Cell Loss Induced by Elevated Intraocular Pressure.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    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

6 authors at 3 institutions in 2 countries.

Ling ZuoDepartment of Ophthalmology, Second Hospital of Jilin University, Jilin, China.
Reas S Khan
Vivian Lee
Kimberly Dine
Wen Wu
Kenneth S Shindler
Penn Presbyterian Medical Center · USUniversity of Pennsylvania · USSecond Affiliated Hospital of Jilin University · CN

Funding

PENN Vision Clinical Scientist ProgramK12EY015398 · NEI · UNIVERSITY OF PENNSYLVANIA · PI JOSHUA L DUNAIEF · 2004 to 2026
$11.7M
Mechanism of SIRT1 Activator Mediated Neuroprotection of Retinal Ganglion CellsR01EY019014 · NEI · UNIVERSITY OF PENNSYLVANIA · PI SHINDLER, KENNETH S · 2010 to 2020
$3.7M
NEI NIH HHS EY019014NEI NIH HHS K12 EY015398NEI NIH HHS R01 EY019014
6 · The paper itself

Abstract

purposeActivation of SIRT1 deacetylase prevents retinal ganglion cell (RGC) loss in experimental optic neuritis, an inflammatory optic neuropathy. While mechanisms of this effect are not known, evidence suggests it involves reduction of oxidative stress. We hypothesized that SIRT1 reduces RGC loss due to oxidative stress in noninflammatory optic neuropathies, and examined effects following traumatic injury.

methodsOptic nerve crush injury was induced in wild-type C57BL/6 mice, mice overexpressing SIRT1, and mice with conditional deletion of SIRT1 in neurons. Wild-type mice were treated daily with vehicle or 250 mg/kg resveratrol, a naturally occurring polyphenol that activates SIRT1. RGC function was assessed by pupillometry and optokinetic responses (OKR), and RGC survival was measured. Superoxide levels were measured to assess oxidative stress.

resultsSignificant decreases in pupillary light responses, OKR and RGC survival occurred 1 week after optic nerve crush, with progressive worsening at 2 to 4 weeks. Resveratrol treatment and SIRT1 overexpression delayed RGC loss and loss of pupillary light responses following optic nerve crush, although no change in RGC loss occurred in neuronal SIRT1-deficient mice. A significant accumulation of superoxide was detected in wild-type optic nerves following crush, and was reduced in mice overexpressing SIRT1 or treated with resveratrol.

conclusionsSIRT1 delays RGC loss following traumatic injury. Effects are associated with reduced oxidative stress. Results suggest SIRT1-activating drugs may have a specific role in preventing traumatic optic nerve damage, and suggest a broader role for this strategy in treating a variety of optic neuropathies that may include a component of oxidative stress.

Indexed as

Oxidative StressAdaptation, BiologicalAnimalsBlotting, WesternCell SurvivalDisease Models, AnimalMiceMice, Inbred C57BLOptic NerveOptic Nerve InjuriesRetinal Ganglion CellsSirtuin 1Sirt1 protein, mouseSirtuin 1neuroprotectionoxidative stressresveratrolretinal ganglion cellsSIRT1traumatic optic neuropathy

Identifiers

PMID23821198
PMCPMC3726244
OpenAlexW1970688878

What OpenQuestion holds

Textmetadata
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.