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Oxidative Stress and the Role of NADPH Oxidase in Glaucoma
Jennifer C Fan Gaskin1, Manisha H Shah1, Elsa C Chan1,2
1Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, East Melbourne 3002, Australia.
Abstract:
Glaucoma is characterised by loss of retinal ganglion cells, and their axons and many pathophysiological processes are postulated to be involved. It is increasingly understood that not one pathway underlies glaucoma aetiology, but rather they occur as a continuum that ultimately results in the apoptosis of retinal ganglion cells. Oxidative stress is recognised as an important mechanism of cell death in many neurodegenerative diseases, including glaucoma. NADPH oxidase (NOX) are enzymes that are widely expressed in vascular and non-vascular cells, and they are unique in that they primarily produce reactive oxygen species (ROS). There is mounting evidence that NOX are an important source of ROS and oxidative stress in glaucoma and other retinal diseases. This review aims to provide a perspective on the complex role of oxidative stress in glaucoma, in particular how NOX expression may influence glaucoma pathogenesis as illustrated by different experimental models of glaucoma and highlights potential therapeutic targets that may offer a novel treatment option to glaucoma patients.
Insights
Oxidative stress, driven by NADPH oxidase (NOX) enzymes, contributes to retinal ganglion cell death in glaucoma. Targeting NOX may offer new therapeutic strategies for this neurodegenerative eye disease.
Area of Science:
- Ophthalmology
- Neuroscience
- Cell Biology
Background:
- Glaucoma involves retinal ganglion cell loss and complex pathophysiological pathways.
- Oxidative stress is a key mechanism in neurodegenerative diseases, including glaucoma.
- NADPH oxidase (NOX) enzymes are significant producers of reactive oxygen species (ROS).
Purpose of the Study:
- To review the role of oxidative stress in glaucoma pathogenesis.
- To explore the influence of NOX expression on glaucoma.
- To identify potential therapeutic targets for glaucoma treatment.
Main Methods:
- Literature review of experimental glaucoma models.
- Analysis of NOX expression and ROS production in retinal diseases.
- Examination of oxidative stress mechanisms in retinal ganglion cell apoptosis.
Main Results:
- Mounting evidence links NOX-derived ROS to oxidative stress in glaucoma.
- NOX enzymes are implicated as a significant source of oxidative damage in the retina.
- Experimental models illustrate the impact of NOX on glaucoma pathogenesis.
Conclusions:
- Oxidative stress plays a complex role in glaucoma.
- NOX enzymes are critical mediators of oxidative stress in glaucoma.
- Targeting NOX pathways presents a promising therapeutic avenue for glaucoma.
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