Evidence map›Paper›PMID 23101909›Full record

ArticleVisual neuroscience2012

Exclusion of aldose reductase as a mediator of ERG deficits in a mouse model of diabetic eye disease.

Ivy S Samuels, Chieh-Allen Lee, J Mark Petrash, Neal S Peachey, Timothy S Kern

Abstract read
In one paragraph

Article in Visual neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

27 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Visual Dysfunction in Diabetes.Annual review of vision science · 2023
    Review
  5. The Role of Aldose Reductase in Beta-Amyloid-Induced Microglia Activation.International journal of molecular sciences · 2022
    Article
  6. OCT imaging of rod mitochondrial respirationExperimental biology and medicine (Maywood, N.J.) · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Observational
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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  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

5 authors at 3 institutions in 1 country.

Ivy S SamuelsResearch Service, Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio 44106, USA. Ivy.Samuels@va.gov
Chieh-Allen Lee
J Mark Petrash
Neal S Peachey
Timothy S Kern
Louis Stokes Cleveland VA Medical Center · USCase Western Reserve University · USUniversity of Colorado Denver · US

Funding

WASHINGTON UNIVERSITY CENTER VISION RESEARCHP30EY002687 · NEI · WASHINGTON UNIVERSITY · PI Philip Andrew Ruzycki · 1985 to 2026
$18.4M
MOLECULAR BIOLOGY OF ALDOSE REDUCTASE AND CATARACTR01EY005856 · NEI · WASHINGTON UNIVERSITY · PI PETRASH, JONATHAN MARK · 1988 to 2014
$6.8M
STUDY OF DIABETIC RETINOPATHYR01EY000300 · NEI · UNIVERSITY OF WISCONSIN MADISON · PI KERN, TIMOTHY S · 1985 to 2013
$4.7M
NEI NIH HHS P30 EY002687NEI NIH HHS R01 EY000300NEI NIH HHS R01 EY00300NEI NIH HHS R01 EY005856
6 · The paper itself

Abstract

Streptozotocin (STZ)-induced diabetes is associated with reductions in the electrical response of the outer retina and retinal pigment epithelium (RPE) to light. Aldose reductase (AR) is the first enzyme required in the polyol-mediated metabolism of glucose, and AR inhibitors have been shown to improve diabetes-induced electroretinogram (ERG) defects. Here, we used control and AR -/- mice to determine if genetic inactivation of this enzyme likewise inhibits retinal electrophysiological defects observed in a mouse model of type 1 diabetes. STZ was used to induce hyperglycemia and type 1 diabetes. Diabetic and age-matched nondiabetic controls of each genotype were maintained for 22 weeks, after which ERGs were used to measure the light-evoked components of the RPE (dc-ERG) and the neural retina (a-wave, b-wave). In comparison to their nondiabetic controls, wildtype (WT) and AR -/- diabetic mice displayed significant decreases in the c-wave, fast oscillation, and off response components of the dc-ERG but not in the light peak response. Nondiabetic AR -/- mice displayed larger ERG component amplitudes than did nondiabetic WT mice; however, the amplitude of dc-ERG components in diabetic AR -/- animals were similar to WT diabetics. ERG a-wave amplitudes were not reduced in either diabetic group, but b-wave amplitudes were lower in WT and AR -/-diabetic mice. These findings demonstrate that the light-induced responses of the RPE and outer retina are disrupted in diabetic mice, but these defects are not due to photoreceptor dysfunction, nor are they ameliorated by deletion of AR. This latter finding suggests that benefits observed in other studies utilizing pharmacological inhibitors of AR might have been secondary to off-target effects of the drugs.

Indexed as

Aldehyde ReductaseDiabetes Mellitus, ExperimentalDiabetic RetinopathyRetinal Pigment EpitheliumAnimalsDisease Models, AnimalElectroretinographyMaleMiceMice, Inbred C57BLMice, KnockoutStreptozocinAldehyde ReductaseStreptozocin

Identifiers

PMID23101909
PMCPMC3745719
OpenAlexW2005391194

What OpenQuestion holds

Textmetadata
LicenceTDM
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.