ArticleVisual neuroscience2017
Loss of CD40 attenuates experimental diabetes-induced retinal inflammation but does not protect mice from electroretinogram defects.
Article in Visual neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Advances in the Role of the CD40-CD154 Pathway in the Pathogenesis of Diabetic Retinopathy.International journal of molecular sciences · 2026Review
- Methylglyoxal: A Key Factor for Diabetic Retinopathy and Its Effects on Retinal Damage.Biomedicines · 2024Review
- Pediatric Type 1 Diabetes: Mechanisms and Impact of Technologies on Comorbidities and Life Expectancy.International journal of molecular sciences · 2023Review
- Endothelial Dysfunction in Diabetic Retinopathy.Frontiers in endocrinology · 2020Review
- The Role of Inflammation in Diabetic Retinopathy.Frontiers in immunology · 2020Review
- Montelukast Prevents Early Diabetic Retinopathy in Mice.Diabetes · 2019Article
- Endogenous insulin signaling in the RPE contributes to the maintenance of rod photoreceptor function in diabetes.Experimental eye research · 2019Article
- Critical role of endoplasmic reticulum stress in chronic endothelial activation-induced visual deficits in tie2-tumor necrosis factor mice.Journal of cellular biochemistry · 2018Article
- Role of Inflammation in Diabetic Retinopathy.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic low grade inflammation is considered to contribute to the development of experimental diabetic retinopathy (DR). We recently demonstrated that lack of CD40 in mice ameliorates the upregulation of inflammatory molecules in the diabetic retina and prevented capillary degeneration, a hallmark of experimental diabetic retinopathy. Herein, we investigated the contribution of CD40 to diabetes-induced reductions in retinal function via the electroretinogram (ERG) to determine if inflammation plays a role in the development of ERG defects associated with diabetes. We demonstrate that diabetic CD40-/- mice are not protected from reduction to the ERG b-wave despite failing to upregulate inflammatory molecules in the retina. Our data therefore supports the hypothesis that retinal dysfunction found in diabetics occurs independent of the induction of inflammatory processes.
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Registered trials
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 Socratic graph.