ArticleGlia2015
Increased mitochondrial fission and volume density by blocking glutamate excitotoxicity protect glaucomatous optic nerve head astrocytes.
Article in Glia, 2015. 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, 62 citations in OpenAlex.
- UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis.Nature metabolism · 2026Article
- Ferroptosis and retinal ganglion cell death in glaucoma: Mechanisms and therapeutic approaches.Journal of pharmaceutical analysis · 2026Review
- AAV-NDI1 Therapy Provides Significant Benefit to Murine and Cellular Models of Glaucoma.International journal of molecular sciences · 2024Article
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- The role of TRPV4 in the regulation of retinal ganglion cells apoptosis in rat and mouse.Heliyon · 2023Article
- Role of A-Kinase Anchoring Protein 1 in Retinal Ganglion Cells: Neurodegeneration and Neuroprotection.Cells · 2023Review
- Individual astrocyte morphology in the collagenous lamina cribrosa revealed by multicolor DiOlistic labeling.Experimental eye research · 2023Article
- Translatomic response of retinal Müller glia to acute and chronic stress.Neurobiology of disease · 2022Article
- Glaucoma-TrEl: A web-based interactive database to build evidence-based hypotheses on the role of trace elements in glaucoma.BMC research notes · 2022Article
- Review
- The Intertwined Roles of Oxidative Stress and Endoplasmic Reticulum Stress in Glaucoma.Antioxidants (Basel, Switzerland) · 2022Review
- Degeneration of retina-brain components and connections in glaucoma: Disease causation and treatment options for eyesight preservation.Current research in neurobiology · 2022Review
- Review
- cAMP/PKA pathway and mitochondrial protection in oxidative stress-induced optic nerve head astrocytes.Neural regeneration research · 2021Article
- Therapeutic Drugs and Devices for Tackling Ocular Hypertension and Glaucoma, and Need for Neuroprotection and Cytoprotective Therapies.Frontiers in pharmacology · 2021Review
- Memantine ameliorates motor impairments and pathologies in a mouse model of neuromyelitis optica spectrum disorders.Journal of neuroinflammation · 2020Article
- Resveratrol Protects Optic Nerve Head Astrocytes from Oxidative Stress-Induced Cell Death by Preventing Caspase-3 Activation, Tau Dephosphorylation at SerCellular and molecular neurobiology · 2020Article
- Transgenic models for investigating the nervous system: Currently available neurofluorescent reporters and potential neuronal markers.Biochimica et biophysica acta. General subjects · 2020Review
- Loss of AKAP1 triggers Drp1 dephosphorylation-mediated mitochondrial fission and loss in retinal ganglion cells.Cell death & disease · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Abnormal structure and function of astrocytes have been observed within the lamina cribrosa region of the optic nerve head (ONH) in glaucomatous neurodegeneration. Glutamate excitotoxicity-mediated mitochondrial alteration has been implicated in experimental glaucoma. However, the relationships among glutamate excitotoxicity, mitochondrial alteration and ONH astrocytes in the pathogenesis of glaucoma remain unknown. We found that functional N-methyl-d-aspartate (NMDA) receptors (NRs) are present in human ONH astrocytes and that glaucomatous human ONH astrocytes have increased expression levels of NRs and the glutamate aspartate transporter. Glaucomatous human ONH astrocytes exhibit mitochondrial fission that is linked to increased expression of dynamin-related protein 1 and its phosphorylation at Serine 616. In BAC ALDH1L1 eGFP or Thy1-CFP transgenic mice, NMDA treatment induced axon loss as well as hypertrophic morphology and mitochondrial fission in astrocytes of the glial lamina. In human ONH astrocytes, NMDA treatment in vitro triggered mitochondrial fission by decreasing mitochondrial length and number, thereby reducing mitochondrial volume density. However, blocking excitotoxicity by memantine (MEM) prevented these alterations by increasing mitochondrial length, number and volume density. In glaucomatous DBA/2J (D2) mice, blocking excitotoxicity by MEM inhibited the morphological alteration as well as increased mitochondrial number and volume density in astrocytes of the glial lamina. However, blocking excitotoxicity decreased autophagosome/autolysosome volume density in both astrocytes and axons in the glial lamina of glaucomatous D2 mice. These findings provide evidence that blocking excitotoxicity prevents ONH astrocyte dysfunction in glaucomatous neurodegeneration by increasing mitochondrial fission, increasing mitochondrial volume density and length, and decreasing autophagosome/autolysosome formation. GLIA 2015;63:736-753.
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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.