Evidence map›Paper›PMID 20162412›Full record

ArticleDiabetologia2010

Neurodegenerative influence of oxidative stress in the retina of a murine model of diabetes.

M Sasaki, Y Ozawa, T Kurihara, S Kubota, K Yuki, K Noda, S Kobayashi, S Ishida, K Tsubota

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetologia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 3 pooled it
9.4field-weighted citation impact, top 1% 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

148 citing papers in PubMed, 3 syntheses or guidelines pooled it, 288 citations in OpenAlex.

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  17. Retinal Neurodegeneration in an Intraocular Pressure Fluctuation Rat Model.International journal of molecular sciences · 2024
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88 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

9 authors at 3 institutions in 1 country.

M SasakiLaboratory of Retinal Cell Biology, Keio University School of Medicine, Tokyo, Japan.
Y Ozawa
T Kurihara
S Kubota
K Yuki
K Noda
S Kobayashi
S Ishida
K Tsubota
Keio University Hospital · JPKeio University · JPHokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisDiabetic retinopathy is a progressive neurodegenerative disease, but the underlying mechanism is still obscure. Here, we focused on oxidative stress in the retina, and analysed its influence on retinal neurodegeneration, using an antioxidant, lutein.

methodsC57BL/6 mice with streptozotocin-induced diabetes were constantly fed either a lutein-supplemented diet or a control diet from the onset of diabetes, and their metabolic data were recorded. In 1-month-diabetic mice, reactive oxygen species (ROS) in the retina were measured using dihydroethidium and visual function was evaluated by electroretinograms. Levels of activated extracellular signal-regulated kinase (ERK), synaptophysin and brain-derived neurotrophic factor (BDNF) were also measured by immunoblotting in the retina of 1-month-diabetic mice. In the retinal sections of 4-month-diabetic mice, histological changes, cleaved caspase-3 and TUNEL staining were analysed.

resultsLutein did not affect the metabolic status of the diabetic mice, but it prevented ROS generation in the retina and the visual impairment induced by diabetes. ERK activation, the subsequent synaptophysin reduction, and the BDNF depletion in the diabetic retina were all prevented by lutein. Later, in 4-month-diabetic mice, a decrease in the thickness of the inner plexiform and nuclear layers, and ganglion cell number, together with increase in cleaved caspase-3- and TUNEL-positive cells, were avoided in the retina of lutein-fed mice. CONCLUSIONS/

interpretationThe results indicated that local oxidative stress that has a neurodegenerative influence in the diabetic retina is prevented by constant intake of a lutein-supplemented diet. The antioxidant, lutein may be a potential therapeutic approach to protect visual function in diabetes.

Indexed as

Dietary SupplementsAnalysis of VarianceAnimalsBlotting, WesternBrain-Derived Neurotrophic FactorDiabetes Mellitus, ExperimentalDiabetic RetinopathyExtracellular Signal-Regulated MAP KinasesLuteinMiceNerve DegenerationOxidative StressReactive Oxygen SpeciesRetinaSynaptophysinBrain-Derived Neurotrophic FactorExtracellular Signal-Regulated MAP KinasesLuteinReactive Oxygen SpeciesSynaptophysin

Identifiers

PMID20162412
PMCPMC2850533
OpenAlexW1994148925

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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.