ArticleDiabetologia2015
Role of the receptor for advanced glycation endproducts (RAGE) in retinal vasodegenerative pathology during diabetes in mice.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.
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Who cites it
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.
- Effects of diabetes on microglial physiology: a systematic review of in vitro, preclinical and clinical studies.Journal of neuroinflammation · 2023Pooled it
- Association of genetic variants in the receptor for advanced glycation end products gene with diabetic retinopathy: A meta-analysis.Medicine · 2016Pooled it
- Models of hyperglycaemia in diabetes mellitus and its complications.Nature reviews. Endocrinology · 2026Review
- A Time-Programmed Bilayer Wound Dressing for Dynamic Microenvironment Modulation and Full-Thickness Regeneration in Diabetic Wounds.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Forns index and fatty liver index, but not FIB-4, are associated with indices of glycaemia, pre-diabetes and type 2 diabetes: analysis of The Maastricht Study.BMJ open gastroenterology · 2024Article
- Candidate SNP Markers Significantly Altering the Affinity of the TATA-Binding Protein for the Promoters of Human Genes Associated with Primary Open-Angle Glaucoma.International journal of molecular sciences · 2024Article
- Methylglyoxal: A Key Factor for Diabetic Retinopathy and Its Effects on Retinal Damage.Biomedicines · 2024Review
- The contribution of adiponectin to diabetic retinopathy progression: Association with the AGEs-RAGE pathway.Heliyon · 2024Article
- Glycative stress as a cause of macular degeneration.Progress in retinal and eye research · 2024Review
- Exploring the Associated Genetic Causes of Diabetic Retinopathy as a Model of Inflammation in Retinal Diseases.International journal of molecular sciences · 2024Article
- NOD1 deficiency ameliorates the progression of diabetic retinopathy by modulating bone marrow-retina crosstalk.Stem cell research & therapy · 2024Article
- Article
- Manifestation of Pathology in Animal Models of Diabetic Retinopathy Is Delayed from the Onset of Diabetes.International journal of molecular sciences · 2024Review
- The effect of GLP-1 receptor agonist lixisenatide on experimental diabetic retinopathy.Acta diabetologica · 2023Article
- Subendothelial Matrix Stiffening by Lysyl Oxidase Enhances RAGE-Mediated Retinal Endothelial Activation in Diabetes.Diabetes · 2023Article
- Activation of oxytocin receptors in mouse GABAergic amacrine cells modulates retinal dopaminergic signaling.BMC biology · 2022Article
- The RAGE/DIAPH1 Signaling Axis & Implications for the Pathogenesis of Diabetic Complications.International journal of molecular sciences · 2022Review
- Molecular Characteristics of RAGE and Advances in Small-Molecule Inhibitors.International journal of molecular sciences · 2021Review
- Patrolling Monocytes Are Recruited and Activated by Diabetes to Protect Retinal Microvessels.Diabetes · 2020Article
- Glyoxalase System as a Therapeutic Target against Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe receptor for AGEs (RAGE) is linked to proinflammatory pathology in a range of tissues. The objective of this study was to assess the potential modulatory role of RAGE in diabetic retinopathy.
methodsDiabetes was induced in wild-type (WT) and Rage (-/-) mice (also known as Ager (-/-) mice) using streptozotocin while non-diabetic control mice received saline. For all groups, blood glucose, HbA1c and retinal levels of methylglyoxal (MG) were evaluated up to 24 weeks post diabetes induction. After mice were killed, retinal glia and microglial activation, vasopermeability, leucostasis and degenerative microvasculature changes were determined.
resultsRetinal expression of RAGE in WT diabetic mice was increased after 12 weeks (p < 0.01) but not after 24 weeks. Rage (-/-) mice showed comparable diabetes but accumulated less MG and this corresponded to enhanced activity of the MG-detoxifying enzyme glyoxalase I in their retina when compared with WT mice. Diabetic Rage (-/-) mice showed significantly less vasopermeability, leucostasis and microglial activation (p < 0.05-0.001). Rage (-/-) mice were also protected against diabetes-related retinal acellular capillary formation (p < 0.001) but not against pericyte loss. CONCLUSIONS/
interpretationRage (-/-) in diabetic mice is protective against many retinopathic lesions, especially those related to innate immune responses. Inhibition of RAGE could be a therapeutic option to prevent diabetic retinopathy.
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