Lowering IOP does not completely halt progression of glaucoma. Thus, it is important to identify neuroprotective therapies aimed at reducing RGC death. Although the pathogenesis underlying glaucomatous RGC damage remains unclear, mitochondrial dysfunction induced by IOP elevation and oxidative stress is considered as one of major causal factors in glaucomatous neurodegeneration.
Coenzyme Q10 (CoQ10) is an essential electron carrier in mitochondrial respiratory chain complexes and involved in antioxidant mechanisms. It has been reported that ubiquinol, the reduced and active form of CoQ10, is a neuroprotectant in several neuro-degenerative diseases including Alzheimer's disease, traumatic brain injury, and multiple system atrophy.
In the present study, authors investigated whether ubiquinol supplementation promoted RGC survival as well as preserved visual function against oxidative stress using a chronic mouse model of glaucoma, DBA/2J mice. As a result, a diet supplementation with ubiquinol significantly enhanced RGC survival. Authors also demonstrated that ubiquinol significantly blocked BAX activation and increased expression of transcription factor A (TFAM) and activation of oxidative phosphorylation (OXPHOS) complex. TFAM is associated with endogenous repair mechanisms of damaged retinal neurons. OXPHOS complex II is considered to promote cell survival.
Ubiquinol protects RGCs
Therefore, these findings demonstrate that ubiquinol protects RGCs by modulating the BAX-mediated apoptotic pathway and by increasing TFAM expression and OXPHOS complex II activity in glaucomatous neurodegeneration. Additionally, ubiquinol ameliorated RGC death and visual dysfunction in mice against oxidative stress.
Taken together, authors provide us encouraging results indicating that ubiquinol has a therapeutic potential for treating oxidative stress-associated glaucomatous neurodegeneration.