Oxidative stress and mitochondrial dysfunction in glaucoma

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.

Graphical abstractDownload high-res image (157KB)Download full-size imageHighlights► Oxidative stress is thought to contribute to the pathogenesis of glaucoma. ► Mitochondria are a central source and target of oxidative stress. ► Signs of oxidative stress and damage are present in glaucomatous tissue. ► Reactive oxygen species can cause retinal ganglion cell death directly or indirectly. ► Mitochondrial antioxidants may improve disease outcomes in glaucoma.