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Curr Opin Pharmacol. 2013 Feb;13(1):12-5. doi: 10.1016/j.coph.2012.09.008. Epub 2012 Oct 12.

Oxidative stress and mitochondrial dysfunction in glaucoma.

Author information

1
Centre for Eye Research Australia, The University of Melbourne, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC 3002, Australia.

Abstract

Mitochondrial dysfunction increases reactive oxygen species (ROS) production and when this overwhelms the cellular antioxidant defences, oxidative stress ensues. Oxidative stress is recognized as a common pathologic pathway in many neurodegenerative diseases. Recent reports have also demonstrated oxidative stress in ocular tissues derived from experimental glaucoma models and clinical samples. There is also accumulating evidence pointing to mitochondrial dysfunction being present in some glaucoma patients. Thus oxidative stress from mitochondrial dysfunction may also play a causal role in glaucoma. The mechanisms by which oxidative stress may induce retinal ganglion cell loss in glaucoma are not fully understood but could include direct neurotoxic effects from ROS or indirect damage from oxidative stress-induced dysfunction of glial cells. This review will consider the evidence for the presence of oxidative stress in glaucoma; the mechanisms by which oxidative stress may contribute to disease pathogenesis; and also consider therapeutic approaches that target oxidative stress as a means of protecting against optic nerve degeneration.

PMID:
23069478
DOI:
10.1016/j.coph.2012.09.008
[Indexed for MEDLINE]

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