Evidence map›Paper›PMID 24733965›Full record

ArticleMediators of inflammation2014

The proinflammatory cytokine high-mobility group box-1 mediates retinal neuropathy induced by diabetes.

Ahmed M Abu El-Asrar, Mohammad Mairaj Siddiquei, Mohd Imtiaz Nawaz, Karel Geboes, Ghulam Mohammad

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In one paragraph

Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 51 citations in OpenAlex.

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  17. PKA regulates HMGB1 through activation of IGFBP-3 and SIRT1 in human retinal endothelial cells cultured in high glucose.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
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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 3 institutions in 2 countries.

Ahmed M Abu El-AsrarDepartment of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia ; Department of Ophthalmology, King Abdulaziz University Hospital, Old Airport Road, P.O. Box 245, Riyadh 11411, Saudi Arabia.ORCID 0000-0003-2226-8617
Mohammad Mairaj SiddiqueiDepartment of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Mohd Imtiaz NawazDepartment of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Karel GeboesLaboratory of Histochemistry and Cytochemistry, University of Leuven, Leuven, Belgium.ORCID 0000-0003-1132-1080
Ghulam MohammadDepartment of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
King Saud University · SAKing Abdulaziz University · SAKU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To test the hypothesis that increased expression of proinflammatory cytokine high-mobility group box-1 (HMGB1) in epiretinal membranes and vitreous fluid from patients with proliferative diabetic retinopathy and in retinas of diabetic rats plays a pathogenetic role in mediating diabetes-induced retinal neuropathy. Retinas of 1-month diabetic rats and HMGB1 intravitreally injected normal rats were studied using Western blot analysis, RT-PCR and glutamate assay. In addition, we studied the effect of the HMGB1 inhibitor glycyrrhizin on diabetes-induced biochemical changes in the retina. Diabetes and intravitreal injection of HMGB1 in normal rats induced significant upregulation of HMGB1 protein and mRNA, activated extracellular signal-regulated kinase 1 and 2 (ERK1/2), cleaved caspase-3 and glutamate; and significant downregulation of synaptophysin, tyrosine hydroxylase, glutamine synthetase, and glyoxalase 1. Constant glycyrrhizin intake from the onset of diabetes did not affect the metabolic status of the diabetic rats, but it significantly attenuated diabetes-induced upregulation of HMGB1 protein and mRNA, activated ERK1/2, cleaved caspase-3, and glutamate. In the glycyrrhizin-fed diabetic rats, the decrease in synaptophysin, tyrosine hydroxylase, and glyoxalase 1 caused by diabetes was significantly attenuated. These findings suggest that early retinal neuropathy of diabetes involves upregulated expression of HMGB1 and can be ameliorated by inhibition of HMGB1.

Indexed as

AnimalsCytokinesDiabetes Mellitus, ExperimentalDiabetic RetinopathyGlutamate-Ammonia LigaseGlycyrrhizic AcidHMGB1 ProteinInflammationLactoylglutathione LyaseMaleRatsRats, Sprague-DawleyRetinaSynaptophysinTyrosine 3-MonooxygenaseCytokinesGlutamate-Ammonia LigaseGlycyrrhizic AcidHbp1 protein, ratHMGB1 ProteinLactoylglutathione LyaseSynaptophysinSyp protein, ratTyrosine 3-Monooxygenase

Identifiers

PMID24733965
PMCPMC3964896
OpenAlexW2034112923

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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.