ArticleNature communications2024
Protein O-GlcNAcylation coupled to Hippo signaling drives vascular dysfunction in diabetic retinopathy.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Lactate-induced MBD2 K186 lactylation promotes YAP1-dependent myofibroblast-like remodeling of Müller cells in diabetic retinopathy.Molecular biomedicine · 2026Article
- Glycosylation of the retina.Biochemical Society transactions · 2026Review
- Review
- RBM15 promotes hyperglycemia-induced retinal endothelial cell injury by regulating FOXO3 stability via m6A modification.Molecular and cellular biochemistry · 2026Article
- Recent advancements in sample pretreatment methods for glycoproteomics.Biophysics reports · 2026Article
- Metabolic Reprogramming-Driven Cardiovascular Immune Damage: From Glyco-Lipotoxicity and Epigenetic Memory to Multidimensional Cross-Organ Communication Networks.International journal of molecular sciences · 2026Review
- Disrupting VE-cadherin Y685 phosphorylation inhibits development of experimental diabetic and prediabetic retinopathy.The Journal of clinical investigation · 2026Article
- KDM6A promotes diabetic retinopathy via H3K27me3-dependent ferroptosis in Müller cells.Cell death & disease · 2026Article
- CircPBX1 ameliorates metabolic memory-associated erectile dysfunction via miR-195-5p/YAP1-mediated angiogenesis in diabetic rats.Communications biology · 2026Article
- Post-translational Modifications in Proteins: Prediction Methods, Biological Functions, and Diseases.MedComm · 2026Review
- Endothelial UNC5B regulates blood‑retinal barrier homeostasis.International journal of molecular medicine · 2026Article
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
- Human Umbilical Cord Mesenchymal Stem Cells Protect Against Steroid-Induced Osteonecrosis of the Femoral Head Through Hippo Pathway.Biomedicines · 2026Article
- Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- O-GlcNAcylation of YAP1 promotes lung transplant ischemia-reperfusion injury via binding to HIF1α transcription factor and activating autophagy and mitophagy.Cell death & disease · 2026Article
- Article
- Lactylation at H3K18 drives pathological angiogenesis via metabolic-epigenetic crosstalk in ischemic retinopathy.Theranostics · 2026Article
- Advanced Glycation End Products and Metabolic-Mechanical Coupling in Diabetic Retinopathy.Clinical ophthalmology (Auckland, N.Z.) · 2026Review
- Glycosylation-Associated Macrophage Signatures Define a Diagnostic Model for Diabetic Retinopathy via Single-Cell Analysis.Journal of ophthalmology · 2026Article
- Curcumin protects the diabetic mouse retina by modulating the Hippo-YAP signaling pathway.International journal of ophthalmology · 2026Article
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Authors and funding
23 authors.
Funding
Abstract
Metabolic disorder significantly contributes to diabetic vascular complications, including diabetic retinopathy, the leading cause of blindness in the working-age population. However, the molecular mechanisms by which disturbed metabolic homeostasis causes vascular dysfunction in diabetic retinopathy remain unclear. O-GlcNAcylation modification acts as a nutrient sensor particularly sensitive to ambient glucose. Here, we observe pronounced O-GlcNAc elevation in retina endothelial cells of diabetic retinopathy patients and mouse models. Endothelial-specific depletion or pharmacological inhibition of O-GlcNAc transferase effectively mitigates vascular dysfunction. Mechanistically, we find that Yes-associated protein (YAP) and Transcriptional co-activator with PDZ-binding motif (TAZ), key effectors of the Hippo pathway, are O-GlcNAcylated in diabetic retinopathy. We identify threonine 383 as an O-GlcNAc site on YAP, which inhibits its phosphorylation at serine 397, leading to its stabilization and activation, thereby promoting vascular dysfunction by inducing a pro-angiogenic and glucose metabolic transcriptional program. This work emphasizes the critical role of the O-GlcNAc-Hippo axis in the pathogenesis of diabetic retinopathy and suggests its potential as a therapeutic target.
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