Abstract
Ocular diseases associated with retinal ganglion cell (RGC) degeneration is the most common neurodegenerative disorder that causes irreversible blindness worldwide. It is characterized by visual field defects and progressive optic nerve atrophy. The underlying pathophysiology and mechanisms of RGC degeneration in several ocular diseases remain largely unknown. RGCs are a population of central nervous system neurons, with their soma located in the retina and long axons that extend through the optic nerve to form distal terminals and connections in the brain. Because of this unique cytoarchitecture and highly compartmentalized energy demand, RGCs are highly mitochondrial-dependent for adenosine triphosphate (ATP) production. Recently, oxidative stress and mitochondrial dysfunction have been found to be the principal mechanisms in RGC degeneration as well as in other neurodegenerative disorders. Here, we review the role of oxidative stress in several ocular diseases associated with RGC degenerations, including glaucoma, hereditary optic atrophy, inflammatory optic neuritis, ischemic optic neuropathy, traumatic optic neuropathy, and drug toxicity. We also review experimental approaches using cell and animal models for research on the underlying mechanisms of RGC degeneration. Lastly, we discuss the application of antioxidants as a potential future therapy for the ocular diseases associated with RGC degenerations.
Highlights
Retinal ganglion cells (RGCs) have multiple functions including the communication between photoreceptors and the brain, processing visual signals, and controlling visual information. [1,2,3]
As several cell and animal models have been used to investigate the role of oxidative stress in RGC degeneration, here, we review the critical experimental models used in the aforementioned investigations
A rat model of anterior ischemic optic neuropathy is a well-established animal model that recapitulates Non-arteritic anterior ischemic optic neuropathy (NAION). rAION can be induced by photodynamic activation of rose Bengal, which produces free radical oxygen at the optic nerve head (ONH) and establishes an environment of oxidative stress leading to ischemic optic neuropathy and subsequent RGC death [173,174,175,176]
Summary
Retinal ganglion cells (RGCs) have multiple functions including the communication between photoreceptors and the brain, processing visual signals, and controlling visual information. [1,2,3]. One reason for the high ATP requirements can be explained by the characteristic of RGCs’ axons, which remain unmyelinated within the retina. Reactive oxidative species (ROS) are generated from the electron transport chain in mitochondria. Homeostasis between the generation and scavenge of ROS can be broken when the electron transport chain or mitochondrial function is impaired [8]. Once the balance of ROS is broken, it can lead to oxidative stress that damages mitochondrial or nuclear chromosomes, compromising cellular function, leading to cell death. We review the latest findings and ongoing experimental studies regarding the role of oxidative stress in eye diseases, that which is related to RGC degeneration in the visual pathway. We further review the various studies investigating antioxidant therapeutics as a treatment for such RGC degenerative eye diseases
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