ArticleCell death & disease2014
Renin-angiotensin system regulates neurodegeneration in a mouse model of normal tension glaucoma.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 57 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
- Effects of Telmisartan on Intraocular Pressure, Blood Pressure, and Ocular Perfusion Pressure in Normal and Glaucomatous Cats.Translational vision science & technology · 2024Article
- Microglial cGAS-STING signaling underlies glaucoma pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Hypertension facilitates age-related diseases. ~ Is hypertension associated with a wide variety of diseases?~.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Review
- Glaucoma and microglia-induced neuroinflammation.Frontiers in ophthalmology · 2023Review
- Nanoparticles for the treatment of glaucoma-associated neuroinflammation.Eye and vision (London, England) · 2022Review
- Angiotensin II Induces Oxidative Stress and Endothelial Dysfunction in Mouse Ophthalmic Arteries via Involvement of AT1 Receptors and NOX2.Antioxidants (Basel, Switzerland) · 2021Article
- Local ocular renin-angiotensin-aldosterone system: any connection with intraocular pressure? A comprehensive review.Annals of medicine · 2020Article
- Receptor-Associated Prorenin System in the Trabecular Meshwork of Patients with Primary Open-Angle Glaucoma and Neovascular Glaucoma.Journal of clinical medicine · 2020Article
- Telmisartan Reduces Axon Degeneration in Mice With Experimental Glaucoma.Investigative ophthalmology & visual science · 2020Article
- Normal tension glaucoma-like degeneration of the visual system in aged marmosets.Scientific reports · 2019Article
- Neuroprotective Peptides in Retinal Disease.Journal of clinical medicine · 2019Review
- Recent advances in genetically modified animal models of glaucoma and their roles in drug repositioning.The British journal of ophthalmology · 2019Review
- Differential effects of N-acetylcysteine on retinal degeneration in two mouse models of normal tension glaucoma.Cell death & disease · 2019Article
- Relationships Between Neurodegeneration and Vascular Damage in Diabetic Retinopathy.Frontiers in neuroscience · 2019Review
- Reactive Oxygen Species-Mediated Damage of Retinal Neurons: Drug Development Targets for Therapies of Chronic Neurodegeneration of the Retina.International journal of molecular sciences · 2018Review
- Article
- Loss of SLC25A46 causes neurodegeneration by affecting mitochondrial dynamics and energy production in mice.Human molecular genetics · 2017Article
- Edaravone suppresses retinal ganglion cell death in a mouse model of normal tension glaucoma.Cell death & disease · 2017Article
- Targeting Oxidative Stress for Treatment of Glaucoma and Optic Neuritis.Oxidative medicine and cellular longevity · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glaucoma, one of the leading causes of irreversible blindness, is characterized by progressive degeneration of optic nerves and retinal ganglion cells (RGCs). In the mammalian retina, excitatory amino acid carrier 1 (EAAC1) is expressed in neural cells, including RGCs, and the loss of EAAC1 leads to RGC degeneration without elevated intraocular pressure (IOP). In the present study, we found that expressions of angiotensin II type 1 receptor (AT1-R) and Toll-like receptor 4 (TLR4) are increased in RGCs and retinal Müller glia in EAAC1-deficient (KO) mice. The orally active AT1-R antagonist candesartan suppressed TLR4 and lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) expressions in the EAAC1 KO mouse retina. Sequential in vivo retinal imaging and electrophysiological analysis revealed that treatment with candesartan was effective for RGC protection in EAAC1 KO mice without affecting IOP. In cultured Müller glia, candesartan suppressed LPS-induced iNOS production by inhibiting the TLR4-apoptosis signal-regulating kinase 1 pathway. These results suggest that the renin-angiotensin system is involved in the innate immune responses in both neural and glial cells, which accelerate neural cell death. Our findings raise intriguing possibilities for the management of glaucoma by utilizing widely prescribed drugs for the treatment of high blood pressure, in combination with conventional treatments to lower IOP.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.