ArticleFrontiers in neuroscience2019
Apolipoprotein E-Mimetic Peptide COG1410 Enhances Retinal Ganglion Cell Survival by Attenuating Inflammation and Apoptosis Following TONI.
Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Müller glial cells located in the peripheral retina are more susceptible to high pressure: implications for glaucoma.Cell & bioscience · 2024Article
- Nanoparticles for the treatment of glaucoma-associated neuroinflammation.Eye and vision (London, England) · 2022Review
- Apolipoprotein E mimetic peptide COG1410 combats pandrug-resistantFrontiers in microbiology · 2022Article
- Mesenchymal stem cell-derived extracellular vesicles as a new therapeutic strategy for ocular diseases.World journal of stem cells · 2020Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vision loss after traumatic optic nerve injury (TONI) is considered irreversible because of the retrograde loss of retinal ganglion cells (RGCs), which undergo inflammation and apoptosis. Previous studies have shown that COG1410, a mimic peptide derived from the apolipoprotein E (apoE) receptor binding region, shows neuroprotective activity in acute brain injury. However, the detailed role and mechanisms of COG1410 in RGC survival and vision restoration after TONI are poorly understood. The current study aimed to investigate the effects of COG1410 on inflammation and apoptosis in a mouse model of TONI. The results showed that TONI-induced visual impairment was accompanied by optic nerve inflammation, apoptosis, edema, and RGC apoptosis. COG1410 significantly prevented the decrease in visual from ever occurring, attenuated inflammation and apoptosis, and reduced optic nerve edema and RGC apoptosis compared with vehicle treatment. These data identify protective roles of COG1410 in the inflammatory and apoptotic processes of TONI, as well as strategies for its treatment.
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