Abstract
Mitochondrial dysfunction within the eye contributes to primarily mitochondrial diseases affecting the visual system such as Leber hereditary optic neuropathy (LHON) as well as more common ocular diseases, including glaucoma, diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration (AMD). For these reasons, druggable targets and gene therapies for improving mitochondrial function have been of significant interest within scientific and pharmaceutical endeavors seeking to improve visual outcomes in ocular disease. These therapies modulate mitochondrial functions, including mitochondrial membrane potential and membrane stability, redox signaling and oxidative stress, mitochondrial quality control including fusion/fission and biogenesis/mitophagy, apoptosis, and mitochondrial genetic-based therapies. As of now, several mitochondrial-targeted therapies have been approved in a limited number of countries, including photobiomodulation for AMD, idebenone for LHON, and SkQ1 for dry eye disease. Elamipretide for nonexudative AMD and gene therapy with GS010 for LHON have additionally shown encouraging results within clinical trials.Translational RelevanceMitochondria are viable therapeutic targets for a broad spectrum of ocular diseases.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
