ArticlePharmaceutical biology2021
Edaravone prevents high glucose-induced injury in retinal Müller cells through thioredoxin1 and the PGC-1α/NRF1/TFAM pathway.
Article in Pharmaceutical biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Edaravone Attenuates Retinal Ganglion Cell Ferroptosis Induced by Ischemia Reperfusion via Inhibiting the p38 MAPK/ATF3 Signaling Pathway.Molecular neurobiology · 2026Article
- Edaravone: Advances on cytoprotective effects, pharmacological properties, and mechanisms of action.Pharmacological reviews · 2026Review
- Suppression of cAMP/PKA/CREB signaling ameliorates retinal injury in diabetic retinopathy.The Kaohsiung journal of medical sciences · 2023Article
- Research Progress on Mitochondrial Dysfunction in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextOxidative injury in a high-glucose (HG) environment may be a mechanism of diabetic retinopathy (DR) and edaravone can protect retinal ganglion cells by scavenging ROS.
objectiveTo explore the effect of edaravone on HG-induced injury. MATERIALS AND
methodsFirst, Müller cells were cultured by different concentrations of glucose for different durations to obtain a suitable culture concentrations and duration. Müller cells were then divided into Control, HG + Vehicle, HG + Eda-5 μM, HG + Eda-10 μM, HG + Eda-20 μM, and HG + Eda-40 μM groups. Cells were cultured by 20 mM glucose and different concentrations of edaravone for 72 h.
resultsThe IC DISCUSSION AND
conclusionThese findings provide a new potential approach for the treatment of DR and indicated new molecular targets in the prevention of DR.
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Registered trials
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