Mitochondrial Trafficking by Prohibitin-Kinesin-Myosin- Cadherin Complex in the Eye

Abstract

Disruption of the mitochondrial-nuclear network leads to accelerated aging and age-related diseases, including age-related macular degeneration. The current study tested the hypothesis that mitochondrial morphology could be demonstrated quantitatively using a mathematic model and mitochondrial traicking complex under stress conditions. To test our hypothesis, normal and aberrant mitochondria were examined quantitatively based on mitochondrial size, shape, position, composition, and dynamics. Adaptation of the mitochondrial network to changes in the intracellular oxidation and reduction milieu is critical for the survival of retinal pigment epithelial cells. Our mitochondrial interactome mapping demonstrated that a positive correlation may exist between oxida-tive stress-mediated phosphorylation and age-related disease progression. The current interactome may provide a potential therapeutic approach to treat mitochondria-induced neurodegeneration, including age-related macular degeneration.