ArticleExperimental eye research2014
Retinal ganglion cell (RGC) programmed necrosis contributes to ischemia-reperfusion-induced retinal damage.
Article in Experimental eye research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 100 citations in OpenAlex.
- Blocking apoptosis promotes survival and alters developmental dynamics of human retinal ganglion cells in retinal organoids.Cell reports · 2026Article
- Study on the differential expression of disulfidptosis-related genes and their association with immune regulation in patients with diabetic retinopathy.Scientific reports · 2026Article
- Analysis of retinal ganglion cell subtypes across six different inbred mouse strains.Molecular vision · 2026Article
- Microglial Necroptosis Mediated by RIPK3 Leads to Retinal Ganglion Cell Apoptosis Through the Release of FGF2 After Ischemia/Reperfusion.Journal of molecular neuroscience : MN · 2025Article
- [Molecular neurobiology · 2025Article
- Catalpol Protects Against Retinal Ischemia Through Antioxidation, Anti-Ischemia, Downregulation of β-Catenin, VEGF, and Angiopoietin-2: In Vitro and In Vivo Studies.International journal of molecular sciences · 2025Article
- Sustained Experimental Myopia Exacerbates the Effect of Eye Growth on Retinal Ganglion Cell Density and Function.International journal of molecular sciences · 2025Article
- Artificial intelligence-enabled discovery of a RIPK3 inhibitor with neuroprotective effects in an acute glaucoma mouse model.Chinese medical journal · 2025Article
- Regulated Necrosis in Glaucoma: Focus on Ferroptosis and Pyroptosis.Molecular neurobiology · 2024Review
- Impact of Acute Ocular Hypertension on Retinal Ganglion Cell Loss in Mice.Translational vision science & technology · 2024Article
- Article
- GSK840 Alleviates Retinal Neuronal Injury by Inhibiting RIPK3/MLKL-Mediated RGC Necroptosis After Ischemia/Reperfusion.Investigative ophthalmology & visual science · 2023Article
- Molecular mechanisms of NMDA excitotoxicity in the retina.Scientific reports · 2023Article
- Regulated Cell Death of Retinal Ganglion Cells in Glaucoma: Molecular Insights and Therapeutic Potentials.Cellular and molecular neurobiology · 2023Review
- Various Forms of Programmed Cell Death Are Concurrently Activated in the Population of Retinal Ganglion Cells after Ischemia and Reperfusion.International journal of molecular sciences · 2023Article
- Necroptosis plays a crucial role in the exacerbation of retinal injury after blunt ocular trauma.Neural regeneration research · 2023Article
- PANoptosis-like cell death in ischemia/reperfusion injury of retinal neurons.Neural regeneration research · 2023Article
- Targeting Necroptosis: A Novel Therapeutic Option for Retinal Degenerative Diseases.International journal of biological sciences · 2023Review
- GSK872 and necrostatin-1 protect retinal ganglion cells against necroptosis through inhibition of RIP1/RIP3/MLKL pathway in glutamate-induced retinal excitotoxic model of glaucoma.Journal of neuroinflammation · 2022Article
- Multiple types of programmed necrosis such as necroptosis, pyroptosis, oxytosis/ferroptosis, and parthanatos contribute simultaneously to retinal damage after ischemia-reperfusion.Scientific reports · 2022Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Retinal ischemia-reperfusion (IR) injury remains a common cause of blindness and has a final pathway of retinal ganglion cell (RGC) death by apoptosis and necrosis. RGC apoptosis was intensively studied in IR injury, while RGC necrosis did not receive nearly enough consideration since it was viewed as an accidental and unregulated cellular event. However, there is evidence that necrosis, like apoptosis, can be implemented by a programmed mechanism. In this study, we tested the role of RGC programmed necrosis (necroptosis) in IR-induced retinal injury. We employed the mouse model of retinal IR injury for in vivo experiments. The oxygen and glucose deprivation (OGD) model was used as an IR model in vitro. Primary RGCs were isolated by an immunopanning technique. Necrostatin 1 (Nec1) was used to inhibit necroptosis in in vitro and in vivo experiments. The changes in gene expression were assessed by quantitative RT-PCR. The distribution of proteins in the retina and in RGC cultures was evaluated by immunohistochemistry and immunocytochemistry, respectively. Our data suggest that proteins (Ripk1 and Ripk3), which initiate necroptosis, were present in normal and ischemic RGCs. Treatment with Nec1 significantly reduced retinal damage after IR. Increased RGC survival and reduced RGC necrosis following OGD were observed in Nec1-treated cultures. We found significantly reduced expression of genes coding pro-inflammatory markers Il1b, Ccl5, Cxcl10, Nos2 and Cybb in Nec1-treated ischemic retinas. Thus, our findings suggest that RGC necroptosis contributes to retinal damage after IR through direct loss of cells and induction of associated inflammatory responses.
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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.