Evidence map›Paper›PMID 26721508›Full record

ArticleNeurochemical research2016

Potential Role of Endoplasmic Reticulum Stress in Pathogenesis of Diabetic Retinopathy.

Gustavo Sánchez-Chávez, Ernesto Hernández-Ramírez, Ixchel Osorio-Paz, Claudia Hernández-Espinosa, Rocío Salceda

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Gustavo Sánchez-ChávezDivisión de Neurociencias, Departamento de Neurodesarrollo y Fisiología, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Apdo. Postal 70-253, CP 04510, Mexico, D. F., Mexico.
Ernesto Hernández-RamírezDivisión de Neurociencias, Departamento de Neurodesarrollo y Fisiología, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Apdo. Postal 70-253, CP 04510, Mexico, D. F., Mexico.
Ixchel Osorio-PazDivisión de Neurociencias, Departamento de Neurodesarrollo y Fisiología, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Apdo. Postal 70-253, CP 04510, Mexico, D. F., Mexico.
Claudia Hernández-EspinosaDivisión de Neurociencias, Departamento de Neurodesarrollo y Fisiología, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Apdo. Postal 70-253, CP 04510, Mexico, D. F., Mexico.
Rocío SalcedaDivisión de Neurociencias, Departamento de Neurodesarrollo y Fisiología, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Apdo. Postal 70-253, CP 04510, Mexico, D. F., Mexico. rsalceda@ifc.unam.mx.
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus is a metabolic disease that leads to several complications which include retinopathy. Multiple biochemical abnormalities have been proposed to explain the development of retinopathy, including oxidative stress. Although the existence of oxidative stress has been established in the retina from long standing diabetic animals, pathogenesis and progression of retinopathy remain unclear. In order to gain insight into the pathogenesis of diabetic retinopathy, we analyzed the levels of different oxidative stress biomarkers in the retina at early stages during the progress of streptozotocin-induced diabetes. No significant changes in glutathione content, expression of NADPH-oxidase, levels of lipid peroxidation, nor production of free radicals were observed in the retina up to 45 days of diabetes induction. Likewise, a transient decrease in aconitase activity, parallel to an increase in the superoxide dismutase activity was observed at 20 days of hyperglycemia, suggesting a high capacity of retina to maintain its redox homeostasis, at least at early stages of diabetes. Nonetheless, we found an early and time-dependent increase in the levels of oxidized proteins, which was not affected by the administration of the antioxidant quercetin. Also, positive immunoreactivity to the reticulum stress protein CHOP was found in glial Müller cells of diabetic rat retinas. These findings suggest the occurrence of endoplasmic reticulum stress as a primary event in retina pathogenesis in diabetes.

Indexed as

Endoplasmic Reticulum StressAconitate HydrataseAnimalsBiomarkersDiabetic RetinopathyEpendymoglial CellsFree RadicalsGlutathioneLipid PeroxidationNADPH OxidasesOxidative StressRats, Long-EvansRetinaTranscription Factor CHOPAconitate HydrataseBiomarkersDdit3 protein, ratFree RadicalsGlutathioneNADPH OxidasesTranscription Factor CHOPCarbonylationDiabetesEndoplasmic reticulum stressGlutathioneNOXQuercetinRetinaSuperoxide dismutase

Identifiers

PMID26721508
OpenAlexW2219583012

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.