ReviewCells2021
The Influence of Mitochondrial Dynamics and Function on Retinal Ganglion Cell Susceptibility in Optic Nerve Disease.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Pooled it
- Linezolid-related Optic Nerve Disorders: Insight From a Pharmacovigilance Analysis of the US FDA Adverse Event Reporting System.Open forum infectious diseases · 2025Trial
- Quantitative Flavoprotein Fluorescence Parameters in Retinal and Optic Nerve Diseases: A Scoping Review.Journal of clinical medicine · 2026Review
- Pharmacological restoration of impaired autophagy in retinal ganglion cells prevents abnormal mitochondrial accumulation and glaucomatous neurodegeneration.Molecular neurodegeneration · 2026Article
- Network Analysis of Convergent and Specific Molecular Pathways of Nutraceuticals with Antioxidant and Neuroprotective Potential in Glaucoma.Antioxidants (Basel, Switzerland) · 2026Article
- The mitochondria-targeted peptide HDAP2 reduces mitochondrial loss and retinal ganglion cell degeneration after optic nerve injury.Neuroscience · 2026Article
- Label-free in vivo molecular profiling of the human retina by non-resonant Raman spectroscopy.Communications biology · 2026Article
- Eccentricity-Dependent Reflectivity Rates-of-Change Across the Retina in Intermediate Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2026Article
- Mesenchymal Stromal Cells and Extracellular Vesicles: A Novel Therapeutic Paradigm for Mitochondrial Dysfunctions.International journal of molecular sciences · 2026Review
- Mitochondrial Resilience in Glaucoma: Targeting NADDiseases (Basel, Switzerland) · 2026Article
- Inner Retinal Reflectivity Loss and Concurrent Thickening Predict Short-Term Conversion to Neovascular AMD.Investigative ophthalmology & visual science · 2026Article
- Circulating eNAMPT in Glaucoma: A Semi-Quantitative Plasma Analysis Before and After Nicotinamide Supplementation.Translational vision science & technology · 2026Article
- SS31 protects damaged retinal cells through the AMPK/DRP1 signaling pathway.Molecular vision · 2026Article
- Growth hormone-releasing hormone in retinal disorders and uveitis: an updated review.International journal of ophthalmology · 2026Review
- Pituitary adenylate cyclase-activating polypeptide and mitochondrial homeostasis in neuronal injury: mechanisms and translational prospects.Frontiers in immunology · 2026Review
- Optic nerve injury impairs intrinsic mechanisms underlying electrical activity in a resilient retinal ganglion cell.The Journal of physiology · 2025Article
- Spatiotemporal Immune Dynamics in Experimental Retinal Ganglion Cell Injury Models.Immunity, inflammation and disease · 2025Review
- Modeling human retinal ganglion cell axonal outgrowth, development, and pathology using pluripotent stem cell-based microfluidic platforms.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Glaucomatous retinal ganglion cells: death and protection.International journal of ophthalmology · 2025Review
- The role of RGC degeneration in the pathogenesis of glaucoma.International journal of biological sciences · 2025Review
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 3 institutions in 2 countries.
Funding
Abstract
The important roles of mitochondrial function and dysfunction in the process of neurodegeneration are widely acknowledged. Retinal ganglion cells (RGCs) appear to be a highly vulnerable neuronal cell type in the central nervous system with respect to mitochondrial dysfunction but the actual reasons for this are still incompletely understood. These cells have a unique circumstance where unmyelinated axons must bend nearly 90° to exit the eye and then cross a translaminar pressure gradient before becoming myelinated in the optic nerve. This region, the optic nerve head, contains some of the highest density of mitochondria present in these cells. Glaucoma represents a perfect storm of events occurring at this location, with a combination of changes in the translaminar pressure gradient and reassignment of the metabolic support functions of supporting glia, which appears to apply increased metabolic stress to the RGC axons leading to a failure of axonal transport mechanisms. However, RGCs themselves are also extremely sensitive to genetic mutations, particularly in genes affecting mitochondrial dynamics and mitochondrial clearance. These mutations, which systemically affect the mitochondria in every cell, often lead to an optic neuropathy as the sole pathologic defect in affected patients. This review summarizes knowledge of mitochondrial structure and function, the known energy demands of neurons in general, and places these in the context of normal and pathological characteristics of mitochondria attributed to RGCs.
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.