ArticleFrontiers in neuroscience2019
Progression and Pathology of Traumatic Optic Neuropathy From Repeated Primary Blast Exposure.
Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Peripheral macrophages and T-cells accumulate in the degenerating optic tract after repetitive head impact.Brain, behavior, and immunity · 2026Article
- Impact-acceleration head injury results in optic neuropathy in the thirteen-lined ground squirrel.Communications biology · 2026Article
- Review
- Repetitive hypoxic preconditioning protects retinal ganglion cells against damage caused by exposure to blast.PloS one · 2026Article
- Alterations of Bioactive Lipid Profiles in the Retina Following Traumatic Optic Neuropathy in Mice.Biomolecules · 2025Article
- The molecular mechanisms underlying retinal ganglion cell apoptosis and optic nerve regeneration in glaucoma (Review).International journal of molecular medicine · 2025Review
- Model matters: Differential outcomes in traumatic optic neuropathy pathophysiology between blunt and blast-wave mediated head injuries.Experimental neurology · 2024Article
- Retinal gliosis and phenotypic diversity of intermediate filament induction and remodeling upon acoustic blast overpressure (ABO) exposure to the rat eye.Experimental eye research · 2023Article
- Traumatic Axonal Injury in the Optic Nerve: The Selective Role of SARM1 in the Evolution of Distal Axonopathy.Journal of neurotrauma · 2023Article
- Microfluidic Platforms Promote Polarization of Human-Derived Retinal Ganglion Cells That Model Axonopathy.Translational vision science & technology · 2023Article
- Dynamic Observation of Retinal Response to Pressure Elevation in a Microfluidic Chamber.Analytical chemistry · 2022Article
- Mesenchymal stem cell secretome protects against oxidative stress-induced ocular blast visual pathologies.Experimental eye research · 2022Article
- miR-181d-5p Protects against Retinal Ganglion Cell Death after Blunt Ocular Injury by Regulating NFIA-Medicated Astrocyte Development.Mediators of inflammation · 2022Article
- Analysis of retinal vasculature changes in indirect traumatic optic neuropathy using optic coherence tomography angiography.International journal of ophthalmology · 2022Article
- Role of Oxidative Stress in Ocular Diseases Associated with Retinal Ganglion Cells Degeneration.Antioxidants (Basel, Switzerland) · 2021Review
- Effects of intravitreal injection of siRNA against caspase-2 on retinal and optic nerve degeneration in air blast induced ocular trauma.Scientific reports · 2021Article
- Traumatic brain injury and sight loss in military and veteran populations- a review.Military Medical Research · 2021Review
- Visual deficits after traumatic brain injury.Histology and histopathology · 2021Review
- Axonopathy precedes cell death in ocular damage mediated by blast exposure.Scientific reports · 2021Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Indirect traumatic optic neuropathy (ITON) is a condition that is often associated with traumatic brain injury and can result in significant vision loss due to degeneration of retinal ganglion cell (RGC) axons at the time of injury or within the ensuing weeks. We used a mouse model of eye-directed air-blast exposure to characterize the histopathology of blast-induced ITON. This injury caused a transient elevation of intraocular pressure with subsequent RGC death and axon degeneration that was similar throughout the length of the optic nerve (ON). Deficits in active anterograde axon transport to the superior colliculus accompanied axon degeneration and first appeared in peripheral representations of the retina. Glial area in the ON increased early after injury and involved a later period of additional expansion. The increase in area involved a transient change in astrocyte organization independent of axon degeneration. While levels of many cytokines and chemokines did not change, IL-1α and IL-1β increased in both the ON and retina. In contrast, glaucoma shows distal to proximal axon degeneration with astrocyte remodeling and increases in many cytokines and chemokines. Further, direct traumatic optic neuropathies have a clear site of injury with rapid, progressive axon degeneration and cell death. These data show that blast-induced ITON is a distinct neuropathology from other optic neuropathies.
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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.