ArticleArteriosclerosis, thrombosis, and vascular biology2025
Nrf2 Deficiency in Müller Cells Exacerbates Pathological Neovascularization in Ischemic Retinopathy.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Single-Nucleus RNA Sequencing Highlights Endothelial and Müller Cell ER Stress During Retinal Neovascularization in Vldlr-/- Mouse.Investigative ophthalmology & visual science · 2026Article
- Mononuclear phagocyte-specific cGAS/STING targeting suppresses experimental choroidal neovascularization.JCI insight · 2026Article
- Beneficial Effects of Natural Bioactive Compounds on Eye Health: A Narrative Review.International journal of molecular sciences · 2026Review
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10 authors.
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Abstract
backgroundMüller cells are the major retinal glial cell type and pivotal regulators of pathological neovascularization in ischemic retinopathy. There is great interest in identifying factors that govern Müller cells in vascular regulation. Nrf2 (NF-E2-related factor 2) plays a major protective role in regulating oxidative stress and inflammation. Our group previously discovered that both global and neuroretinal Nrf2 deficiency suppress retinal revascularization and promote pathological neovascularization in a mouse model of oxygen-induced retinopathy. Here, we investigate the cell-intrinsic role of Nrf2 in Müller cells on retinal angiogenesis.
methodsThe role of Müller cell Nrf2 in retinal angiogenesis was investigated in cell culture and the mouse oxygen-induced retinopathy model. Human retinal endothelial cells were cocultured with primary Müller cells transfected with Nrf2 small-interference RNA. Müller cell-specific Nrf2 knockout mice were subjected to oxygen-induced retinopathy. RNA-seq analysis of a Müller cell-specific RiboTag transcriptome was conducted in wild-type and Nrf2-deficient Müller cells.
resultsSilencing Nrf2 in primary Müller cells increased angiogenic activity in retinal endothelial cells. Müller cell-specific Nrf2 deficiency exacerbated pathological neovascularization in oxygen-induced retinopathy, associated with increased Müller cell gliosis and upregulation of retinal Tnfα (tumor necrosis factor alpha). Müller cell Nrf2 deficiency resulted in dysregulation of multiple genes involved in acute-phase response, inflammation, and angiogenesis, including increased expression of
conclusionsNrf2 in Müller cells plays an integral protective role in modulating retinal angiogenesis and inflammatory responses in ischemic retinopathy. Nrf2 is an important regulator of Müller cell state in retinal ischemia and governs the Müller cell transcriptional program, including LCN2, a novel regulator of angiogenesis. This highlights pharmacological activation of Nrf2 as a therapeutic strategy for pathological neovascularization in ischemic retinopathy.
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