Mitochondrial dysfunction as a convergent pathogenic mechanism in ocular diseases: emerging targeted therapeutic strategies

Mitochondria play a crucial role in maintaining cellular homeostasis by performing essential tasks such as energy production, calcium regulation, redox balance, and controlling apoptosis. In ocular tissues that are highly dependent on energy, particularly the retina and optic nerve, mitochondrial dysfunction has been identified as a major contributor to the development of several sight-threatening diseases. For example, in conditions like glaucoma, age-related macular degeneration (AMD), Leber hereditary optic neuropathy (LHON), and diabetic retinopathy (DR), disruptions in mitochondrial function impair cellular energy production, elevate oxidative stress, and trigger apoptotic pathways, all of which accelerate disease progression and vision loss. Thus, targeting mitochondrial dysfunction may present a promising therapeutic approach for these vision-impairing diseases.