ArticleThe Journal of clinical investigation2017
Targeting neuronal gap junctions in mouse retina offers neuroprotection in glaucoma.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
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Who cites it
35 citing papers in PubMed, 42 citations in OpenAlex.
- High Adhesion Superoleophobic Oil Microdroplets to Create Ocular Hypertension In Vivo.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Synaptic control of retinal ganglion cell survival and axon regeneration.Molecular neurodegeneration · 2026Review
- Inhibition of connexin hemichannels protects retinal ganglion cells against ocular nerve injury.Cellular and molecular life sciences : CMLS · 2026Article
- Gap junction protein connexin 36 proteostatic mechanisms in photoreceptor cells subjected to excitotoxic stress.Acta biochimica Polonica · 2026Article
- The Role of Connexin 36 Gap Junctions in Retinal Ganglion Cell Death After Corneal Alkali Burns.Investigative ophthalmology & visual science · 2025Article
- The structure, function, and distribution of gap junctions in the retina: Life cycle in health and disease.Journal of cell communication and signaling · 2025Review
- Targeting Connexin 43 in Retinal Astrocytes Promotes Neuronal Survival in Glaucomatous Injury.Glia · 2025Article
- Targeting Connexins Biology as Therapeutic Strategies Against Retinal Diseases.Advances in experimental medicine and biology · 2025Review
- Mefloquine-induced conformational shift in Cx36 N-terminal helix leading to channel closure mediated by lipid bilayer.Nature communications · 2024Article
- Review: Neuroprotective Nanocarriers in Glaucoma.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Neuroprotection of Retinal Ganglion Cells Suppresses Microglia Activation in a Mouse Model of Glaucoma.Investigative ophthalmology & visual science · 2023Article
- Intraocular nano-microscale drug delivery systems for glaucoma treatment: design strategies and recent progress.Journal of nanobiotechnology · 2023Review
- Connexins Biology in the Pathophysiology of Retinal Diseases.Advances in experimental medicine and biology · 2023Article
- cGMP Signaling in the Neurovascular Unit-Implications for Retinal Ganglion Cell Survival in Glaucoma.Biomolecules · 2022Review
- METTL23 mutation alters histone H3R17 methylation in normal-tension glaucoma.The Journal of clinical investigation · 2022Article
- Association of CX36 Protein Encoding GeneGenes · 2022Article
- A Robust Microbead Occlusion Model of Glaucoma for the Common Marmoset.Translational vision science & technology · 2022Article
- The heterogeneity of astrocytes in glaucoma.Frontiers in neuroanatomy · 2022Review
- Axon hyperexcitability in the contralateral projection following unilateral optic nerve crush in mice.Brain communications · 2022Article
- The role of gap junctions in cell death and neuromodulation in the retina.Neural regeneration research · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The progressive death of retinal ganglion cells and resulting visual deficits are hallmarks of glaucoma, but the underlying mechanisms remain unclear. In many neurodegenerative diseases, cell death induced by primary insult is followed by a wave of secondary loss. Gap junctions (GJs), intercellular channels composed of subunit connexins, can play a major role in secondary cell death by forming conduits through which toxic molecules from dying cells pass to and injure coupled neighbors. Here we have shown that pharmacological blockade of GJs or genetic ablation of connexin 36 (Cx36) subunits, which are highly expressed by retinal neurons, markedly reduced loss of neurons and optic nerve axons in a mouse model of glaucoma. Further, functional parameters that are negatively affected in glaucoma, including the electroretinogram, visual evoked potential, visual spatial acuity, and contrast sensitivity, were maintained at control levels when Cx36 was ablated. Neuronal GJs may thus represent potential therapeutic targets to prevent the progressive neurodegeneration and visual impairment associated with glaucoma.
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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.