ArticleNutrition & diabetes2022
Inhibition of CD40-TRAF6-dependent inflammatory activity halts the onset of diabetic retinopathy in streptozotocin-diabetic mice.
Article in Nutrition & diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Salidroside attenuates diabetic retinopathy by upregulating miR-142-3p to target TRAF6.Journal of molecular histology · 2026Article
- Diabetic Retinopathy, a Comprehensive Overview on Pathophysiology and Relevant Experimental Models.International journal of molecular sciences · 2025Review
- Sex Differences in Inflammatory Plasma Proteins in Patients With Diabetic Retinopathy.Translational vision science & technology · 2025Article
- Unveiling the molecular complexity of proliferative diabetic retinopathy through scRNA-seq, AlphaFold 2, and machine learning.Frontiers in endocrinology · 2024Article
- Anti-IL17A Halts the Onset of Diabetic Retinopathy in Type I and II Diabetic Mice.International journal of molecular sciences · 2023Article
- The role of ceramides in the pathophysiology of diabetic retinopathy: Mechanisms and Implications for therapeutic strategies.Diabetes & vascular disease researchReview
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Diabetes initiates inflammation that can impair the retinal vasculature, and lead to diabetic retinopathy; one of the leading causes of blindness. Inflammatory pathways have been examined as potential therapeutic targets for diabetic retinopathy, but there is still a need for early-stage treatments. We hypothesized that the CD40-TNF Receptor Associated Factor 6 (TRAF6) axis plays a pivotal role in the onset of diabetic retinopathy, and that the CD40-TRAF6 axis would be a prime therapeutic target for early-stage non-proliferative diabetic retinopathy. The CD40-TRAF6 complex can initiate NFκB activation, inflammation, and tissue damage. Further, CD40 and TRAF6 are constitutively expressed on Muller glia, and upregulated in the diabetic retina. Yet the role of the CD40-TRAF6 complex in the onset of diabetic retinopathy is still unclear. In the current study, we examined the CD40-TRAF6 axis in diabetic retinopathy using a small molecule inhibitor (SMI-6877002) on streptozotocin-induced diabetic mice. When CD40-TRAF6-dependent inflammation was inhibited, retinal vascular leakage and capillary degeneration was ameliorated in diabetic mice. Collectively, these data suggest that the CD40-TRAF6 axis plays a pivotal role in the onset of diabetic retinopathy, and could be a novel therapeutic target for early diabetic retinopathy.
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Registered trials
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