ArticleDiabetologia2026
Aberrant STING signalling promotes endothelial dysfunction and neurovascular injury in diabetic retinopathy.
Article in Diabetologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Microglial TSPAN4-Dependent Migrasomes Promote Pathological Retinal Neovascularization via Immune-Vascular Crosstalk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Role of the cGAS-STING signaling pathway in diabetes mellitus and its complications: from mechanisms to therapeutics.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
aims/hypothesisDiabetic retinopathy is a common complication of diabetes mellitus that is characterised by neurovascular dysfunction and chronic inflammation. The stimulator of IFN genes (STING) signalling pathway plays a key role in inflammatory diseases. However, its cell-specific function and value as an early-intervention target for diabetic retinopathy remain unclear.
methodsWe analysed public single-cell (sc)RNA-seq datasets from fibrous membranes of individuals with proliferative diabetic retinopathy and idiopathic macular hole, normal post-mortem retinas and retinal endothelial cells from diabetic and non-diabetic mice. A type 2 diabetes mouse model was established using a high-fat diet and streptozocin to assess STING localisation and expression differences. Using adeno-associated virus (serotype 2/1), siRNA or STING inhibitor H-151, we evaluated the effects of STING on inflammation and cell function both in vivo and in vitro.
resultsscRNA-seq analysis revealed increased STING expression and enriched IFN signalling in endothelial cells from samples of both humans and mice with diabetes. Our mouse model exhibited increased STING expression, along with its co-localisation with CD31, and upregulated IFNs in retinal tissues. Flow cytometry confirmed diabetes-induced endothelial cell-specific phosphorylation of TBK1, a downstream effector of STING. Genetic deletion or pharmacological inhibition of STING significantly ameliorated retinal inflammation and neurovascular dysfunction in diabetic mice. CONCLUSIONS/
interpretationOur findings demonstrate endothelial-intrinsic activation of the cyclic GMP-AMP synthase (cGAS)/STING/IFN pathway as a key driver of retinal inflammation and neurovascular dysfunction in diabetes. Targeting this pathway may offer a potential therapeutic approach for early intervention in diabetic retinopathy.
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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.