Abstract

Mitochondrial optic neuropathy (MON) describes a group of optic neuropathies that exhibit mitochondrial dysfunction in retinal ganglion cells. Pathogenesis of MON includes genetic factors, such as Leber hereditary optic neuropathy and dominant optic atrophy, or acquired factors, such as drug intoxication and nutritional deficiencies, or the combination of both genetic factors and acquired factors. Regardless of different causes, MON shares similar features including bilateral central visual acuity loss, equally normal or slightly sluggish reaction of pupils to light and so on. Many novel therapies, such as pharmacological strategies, genetic therapy and stem cell therapy, are being widely studied in order to limit or reverse the damage of retinal ganglion cells. This article review the pathogenesis, clinical manifestations, ancillary testing, differential diagnosis and treatment progress of MON. (Chin J Ophthalmol, 2021, 57: 386-390).

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