Evidence map›Paper›PMID 33372981›Full record

ArticleInvestigative ophthalmology & visual science2020

Hydrogen Sulfide: A Potential Therapeutic Target in the Development of Diabetic Retinopathy.

Ghulam Mohammad, Rakesh Radhakrishnan, Renu A Kowluru

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  6. Protective Role of HDiabetes, metabolic syndrome and obesity : targets and therapy · 2025
    Review
  7. Linking homocysteine and ferroptosis in cardiovascular disease: insights and implications.Apoptosis : an international journal on programmed cell death · 2024
    Review
  8. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Ghulam MohammadKresge Eye Institute, Wayne State University, Detroit, Michigan, United States.
Rakesh RadhakrishnanKresge Eye Institute, Wayne State University, Detroit, Michigan, United States.
Renu A KowluruKresge Eye Institute, Wayne State University, Detroit, Michigan, United States.
Wayne State University · USKresge Eye Institute · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Role of Ras in Retinal Cell Death in DiabetesR01EY014370 · NEI · WAYNE STATE UNIVERSITY · PI KOWLURU, RENU A. · 2004 to 2023
$4.8M
Glycemic Control and Progression of Diabetic RetinopathyR01EY017313 · NEI · WAYNE STATE UNIVERSITY · PI KOWLURU, RENU A. · 2007 to 2022
$4.2M
NADPH Oxidase, Mitochondrial Dysfunction and Diabetic RetinopathyR01EY022230 · NEI · WAYNE STATE UNIVERSITY · PI KOWLURU, ANJANEYULU, KOWLURU, RENU A. · 2012 to 2022
$3.4M
NEI NIH HHS R01 EY014370NEI NIH HHS R01 EY017313NEI NIH HHS R01 EY022230NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

Purpose: Hyperglycemia damages the retinal mitochondria, and the mitochondrial damage plays a central role in the development of diabetic retinopathy. Patients with diabetes also have higher homocysteine levels, and abnormalities in homocysteine metabolism result in decreased levels of hydrogen sulfide (H2S), an endogenous gasotransmitter signaling molecule with antioxidant properties. This study aimed to investigate the role of H2S in the development of diabetic retinopathy. Methods: Streptozotocin-induced diabetic mice were administered a slow releasing H2S donor GYY4137 for 6 months. The retina was used to measure H2S levels, and their retinal vasculature was analyzed for the histopathology characteristic of diabetic retinopathy and oxidative stress, mitochondrial damaging matrix metalloproteinase-9 (MMP-9), and mitochondrial integrity. These parameters were also measured in the isolated retinal endothelial cells incubated in high glucose medium containing GYY4137. Results: Administration of GYY4137 to diabetic mice ameliorated decrease in H2S and prevented the development of histopathology, characteristic of diabetic retinopathy. Diabetes-induced increase in oxidative stress, MMP-9 activation, and mitochondrial damage were also attenuated in mice receiving GYY4137. Results from isolated retinal endothelial cells confirmed the results obtained from diabetic mice. Conclusions: Thus, supplementation of H2S donor prevents the development of diabetic retinopathy by ameliorating increase in oxidative stress and preserving the mitochondrial integrity. H2S donors may provide a novel therapeutic strategy to inhibit the development of diabetic retinopathy.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalDiabetic RetinopathyFemaleFluorescent Antibody TechniqueHumansHydrogen SulfideMaleMatrix Metalloproteinase 9Membrane Potential, MitochondrialMice, Inbred C57BLMorpholinesOrganothiophosphorus CompoundsOxidative StressReactive Oxygen SpeciesRetinaGYY 4137Hydrogen SulfideMatrix Metalloproteinase 9MorpholinesOrganothiophosphorus CompoundsReactive Oxygen Species

Identifiers

PMID33372981
PMCPMC7774116
OpenAlexW3115391657

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.