Neuroinflammation in Primary Open-Angle Glaucoma

Primary open-angle glaucoma (POAG) is the second leading cause of irreversible blindness worldwide. Increasing evidence suggests oxidative damage and immune response defects are key factors contributing to glaucoma onset. Indeed, both the failure of the trabecular meshwork tissue in the conventional...

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Bibliographic Details
Published in:Journal of clinical medicine 2020-09, Vol.9 (10), p.3172
Main Authors: Vernazza, Stefania, Tirendi, Sara, Bassi, Anna Maria, Traverso, Carlo Enrico, Saccà, Sergio Claudio
Format: Article
Language:English
Subjects:
Aging
Antioxidants
Apoptosis
Blood pressure
Chronic illnesses
Clinical medicine
Diabetic retinopathy
Enzymes
Glaucoma
Mitochondria
Mitochondrial DNA
Mutation
Neurodegeneration
Optic nerve
Oxidative stress
Pathogenesis
Permeability
Proteins
Review
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Summary:Primary open-angle glaucoma (POAG) is the second leading cause of irreversible blindness worldwide. Increasing evidence suggests oxidative damage and immune response defects are key factors contributing to glaucoma onset. Indeed, both the failure of the trabecular meshwork tissue in the conventional outflow pathway and the neuroinflammation process, which drives the neurodegeneration, seem to be linked to the age-related over-production of free radicals (i.e., mitochondrial dysfunction) and to oxidative stress-linked immunostimulatory signaling. Several previous studies have described a wide range of oxidative stress-related makers which are found in glaucomatous patients, including low levels of antioxidant defences, dysfunction/activation of glial cells, the activation of the NF-κB pathway and the up-regulation of pro-inflammatory cytokines, and so on. However, the intraocular pressure is still currently the only risk factor modifiable by medication or glaucoma surgery. This present review aims to summarize the multiple cellular processes, which promote different risk factors in glaucoma including aging, oxidative stress, trabecular meshwork defects, glial activation response, neurodegenerative insults, and the altered regulation of immune response.
ISSN:2077-0383
2077-0383
DOI:10.3390/jcm9103172