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Updated: Mar 27, 2026

Determination of Mitochondrial Respiration and Glycolysis in Ex Vivo Retinal Tissue Samples

Determination of Mitochondrial Respiration and Glycolysis in Ex Vivo Retinal Tissue Samples

Published on: August 4, 2021

Targeting mitochondrial function to protect against vision loss.

Jamuna Chhetri¹, Nuri Gueven¹

¹a Division of Pharmacy, School of Medicine, Faculty of Health , University of Tasmania , Hobart , Australia.

Expert Opinion on Therapeutic Targets

|January 14, 2016

Summary

Mitochondrial dysfunction significantly impacts vision, contributing to various eye diseases. Targeting mitochondria offers a promising therapeutic strategy for preventing vision loss in optic neuropathies.

Keywords:

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

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Area of Science:

Mitochondrial biology
Ophthalmology
Neuroscience

Background:

Mitochondria generate ATP, crucial for cellular energy demands.
High mitochondrial density in the visual system makes it vulnerable to dysfunction.
Mitochondrial impairment is linked to vision loss in various diseases.

Purpose of the Study:

To explore the role of mitochondrial dysfunction in visual disorders.
To investigate novel therapeutic strategies targeting mitochondria for vision protection.

Main Methods:

Review of evidence linking mitochondrial impairment to eye diseases.
Analysis of clinical results in inherited retinal disorders.
Exploration of therapeutic potential for optic neuropathies.

Main Results:

Vision impairment is a common symptom of mitochondrial diseases.
Mitochondrial dysfunction contributes to glaucoma and neurodegenerative vision loss.
Targeting mitochondria shows promise in treating inherited retinal disorders.

Conclusions:

Mitochondrial origin of visual disorders necessitates novel therapeutics.
Modulating mitochondrial function can protect against vision loss.
Mitochondria-targeted therapies may benefit various optic neuropathies.