ArticleBioengineered2021
Investigation on the expression regulation of RIPK1/RIPK3 in the retinal ganglion cells (RGCs) cultured in high glucose.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Study on the differential expression of disulfidptosis-related genes and their association with immune regulation in patients with diabetic retinopathy.Scientific reports · 2026Article
- PANoptosis in diabetic retinopathy: immunological insights into mechanisms and translational therapies.Frontiers in immunology · 2026Review
- Emerging Roles of Regulated Cell Death-mediated Inflammation in Pathophysiology of Ocular Diseases.Journal of ophthalmic & vision research · 2026Review
- 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
- RBM15 promotes m6A methylation and stability of KLF6 mRNA to accelerate pyroptosis of retinal ganglion cells in early-stage diabetic retinopathy.Journal of molecular histology · 2025Article
- Narrative review of comprehensive management strategies for diabetic retinopathy: interdisciplinary approaches and future perspectives.BMJ public health · 2025Review
- Non-Apoptotic Programmed Cell Death as Targets for Diabetic Retinal Neurodegeneration.Pharmaceuticals (Basel, Switzerland) · 2024Review
- RIPK3 and RIPK1 gene expression in pterygium: unveiling molecular insights into pathogenesis.Molecular biology reports · 2024Article
- The role of regulated necrosis in diabetes and its complications.Journal of molecular medicine (Berlin, Germany) · 2024Review
- GSK840 Alleviates Retinal Neuronal Injury by Inhibiting RIPK3/MLKL-Mediated RGC Necroptosis After Ischemia/Reperfusion.Investigative ophthalmology & visual science · 2023Article
- Neurovascular Cell Death and Therapeutic Strategies for Diabetic Retinopathy.International journal of molecular sciences · 2023Review
- Necroptosis plays a crucial role in the exacerbation of retinal injury after blunt ocular trauma.Neural regeneration research · 2023Article
- Augmenter of liver regeneration protects the kidney against ischemia-reperfusion injury by inhibiting necroptosis.Bioengineered · 2022Article
- Targeting Novel Regulated Cell Death: Pyroptosis, Necroptosis, and Ferroptosis in Diabetic Retinopathy.Frontiers in cell and developmental biology · 2022Review
- Downregulation of circ-UBAP2 ameliorates oxidative stress and dysfunctions of human retinal microvascular endothelial cells (hRMECs) via miR-589-5p/EGR1 axis.Bioengineered · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic retinopathy (DR) represents the most typical complication of type 2 diabetes mellitus and one of the most primary oculopathy causing blindness. However, the mechanism of DR remains unknown. RIPK1/RIPK3, as homologous serine/threonine kinases, are key elements in mediating necroptosis and may have functions in DR development. To clarify the relationship between DR and RIPK1/RIPK3, this study established a model of apoptosis using high-glucose induced RGCs, which were treated with 7.5, 19.5, and 35 mM D-glucose for 12, 24, and 48 h, respectively. Subsequently, the expression of RIPK1/RIPK3 was determined and the protective effect of necrostatin-1 on RGCs injury induced by high glucose was explored. The results demonstrated that the expression of RIPK1 and RIPK3 in the cells was increased markedly following 12 h treatment with 19.5 mM D-glucose. Additionally, following an addition of 100 μM necrostatin-1 in 19.5 mM D-glucose medium for RGCs treatment 12 h, the protein expression of RIPK1 and RIPK3 was decreased markedly, and the number of Nissl bodies in cells was increased substantially. The findings of the present study indicated that high glucose could induce the expression of RIPK1/RIPK3, and necrostatin-1 could effectively protect RGCs from D-glucose-induced cell necrosis.
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