ArticleCell death & disease2026
STING activation induces polarized cytokine secretion of IFN-β and IL-17A promoting photoreceptor death and choroidal disruption in age-related macular degeneration.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Non-Erythropoietic EPO (EPO-R76E) Protects RPE Cells from Ferroptosis by Modulating the Labile Iron Pool and NRF2-GPX4 Axis.Antioxidants (Basel, Switzerland) · 2026Article
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24 authors.
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Abstract
Age-related macular degeneration (AMD) represents one of the therapeutic challenges of aging eye diseases. Our investigation reveals the stimulator of interferon genes (STING) pathway as an orchestrator of immune-mediated retinal degeneration, exhibiting biphasic, stage-dependent functionality-providing cytoprotection in healthy tissue but driving pathogenic inflammation during early AMD progression. Through immunohistochemical analysis of human eyes, we demonstrate stage-dependent cytoplasmic STING upregulation with parallel IFN-β activation. Using patient-derived induced pluripotent stem cells-retinal pigment epithelium (iPSC-RPE) from AMD siblings, we discovered polarized cytokine secretion: apical IFN-β triggers photoreceptor apoptosis in human retinal organoids, while basal IL-17A compromises choroidal neovascularization. The Cryba1 conditional knockout (cKO) AMD-like mouse model confirms STING-driven IL-17A expression, while Il17a knock-in mice substantiate vascular alterations. STING activation establishes a pathogenic feed-forward loop between interferons and IL-17A. Single-cell transcriptomics following AAV2-mediated IFN-β overexpression reveals metabolic and phototransduction dysregulation. Both pharmacological STING inhibition with SN-011 and genetic approaches demonstrate therapeutic rescue. Cryba1/Sting double heterozygous (dhet) mice maintain homeostatic gene expression preserving retinal architecture and function. These findings establish STING as the master regulator simultaneously controlling multiple AMD pathologies through spatially organized inflammation, transforming from protective surveillance to pathogenic driver, and identifying a unified therapeutic target with demonstrated functional rescue across multiple experimental paradigms.
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