ArticleJCI insight2017
Purinergic dysregulation causes hypertensive glaucoma-like optic neuropathy.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Rodent Models of Glaucoma: How Mice and Rats Can Help Human Vision Move Out of the Woods and Into the Light.Cells · 2025Review
- The microglial P2YTranslational neurodegeneration · 2024Review
- Glial cells as a promising therapeutic target of glaucoma: beyond the IOP.Frontiers in ophthalmology · 2023Review
- Astrocytic dysfunction induced by ABCA1 deficiency causes optic neuropathy.Science advances · 2022Article
- Mapping the Binding Sites of UDP and Prostaglandin E2 Glyceryl Ester in the Nucleotide Receptor P2YChemMedChem · 2022Article
- The Mlc1 Promoter Directs Müller Cell-specific Gene Expression in the Retina.Translational vision science & technology · 2022Article
- Retina regeneration: lessons from vertebrates.Oxford open neuroscience · 2022Review
- An insight on established retinal injury mechanisms and prevalent retinal stem cell activation pathways in vertebrate models.Animal models and experimental medicine · 2021Review
- Role of animal models in glaucoma research.Neural regeneration research · 2020Article
- Recent advances in genetically modified animal models of glaucoma and their roles in drug repositioning.The British journal of ophthalmology · 2019Review
- A promising drug candidate for the treatment of glaucoma based on a P2Y6-receptor agonist.Purinergic signalling · 2018Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glaucoma is an optic neuropathy characterized by progressive degeneration of retinal ganglion cells (RGCs) and visual loss. Although one of the highest risk factors for glaucoma is elevated intraocular pressure (IOP) and reduction in IOP is the only proven treatment, the mechanism of IOP regulation is poorly understood. We report that the P2Y6 receptor is critical for lowering IOP and that ablation of the P2Y6 gene in mice (P2Y6KO) results in hypertensive glaucoma-like optic neuropathy. Topically applied uridine diphosphate, an endogenous selective agonist for the P2Y6 receptor, decreases IOP. The P2Y6 receptor was expressed in nonpigmented epithelial cells of the ciliary body and controlled aqueous humor dynamics. P2Y6KO mice exhibited sustained elevation of IOP, age-dependent damage to the optic nerve, thinning of ganglion cell plus inner plexiform layers, and a reduction of RGC numbers. These changes in P2Y6KO mice were attenuated by an IOP lowering agent. Consistent with RGC damage, visual functions were impaired in middle-aged P2Y6KO mice. We also found that expression and function of P2Y6 receptors in WT mice were significantly reduced by aging, another important risk factor for glaucoma. In summary, our data show that dysfunctional purinergic signaling causes IOP dysregulation, resulting in glaucomatous optic neuropathy.
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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 OpenQuestion graph.