Targeting mitochondrial function to protect against vision loss

ABSTRACT

Introduction: Mitochondria, essential to multicellular life, convert food into ATP to satisfy cellular energy demands. Since different tissues have different energy requirements, mitochondrial density is high in tissues with high metabolic needs, such as the visual system, which is therefore highly susceptible to limited energy supply as a result of mitochondrial dysfunction.

Areas covered: Vision impairment is a common feature of most mitochondrial diseases. At the same time, there is mounting evidence that mitochondrial impairment contributes to the pathogenesis of major eye diseases such as glaucoma and might also be involved in the reported vision impairment in neurodegenerative disorders such as Alzheimer’s disease.

Expert opinion: Rather than relying on symptomatic treatment, acknowledging the mitochondrial origin of visual disorders in mitochondrial, neurodegenerative and ocular diseases could lead to novel therapeutics that aim to modulate mitochondrial function in order to protect against vision loss. This approach has already shown some promising clinical results in inherited retinal disorders, which supports the idea that targeting mitochondria could also be a treatment option for other optic neuropathies.

KEYWORDS:

• Drugs
• eyes
• inherited mitochondrial disease
• mitochondria
• neurodegenerative disease
• ocular disease
• short-chain quinones
• vision

Article highlights

• Vision impairment is a common feature of most mitochondrial diseases.

• There is mounting evidence that mitochondrial impairment contributes to the pathogenesis of major eye diseases such as glaucoma and might also be involved in the vision impairment in neurodegenerative disorders such as Alzheimer’s disease.

• Embracing the mitochondrial origin of these ophthalmological disorders represents a unique opportunity to develop novel therapies that aim to restore mitochondrial function.

• Some drug candidates that are known to modulate mitochondrial function and restore mitochondrial energy production improved and protected visual acuity in mitochondrial neuropathies.

• Preclinical evidence suggests that these drugs could also be beneficial in larger ophthalmological indications such as glaucoma.

• The proof-of-concept that it is possible to protect vision by positively modulating mitochondrial function represents a promising avenue to treat visual disorders in general.

This box summarizes key points contained in the article.

Acknowledgement

The authors are also grateful to Emeritus Professor Stuart McLean, University of Tasmania for helpful review of the manuscript.

Financial and competing interests disclosure

The authors were supported by internal funding from the University of Tasmania. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.