The goal of my research is to understand how mitochondrial dysfunction impacts on eye disease and whether it can be targeted for therapy. Irreversible mitochondrial dysfunction involves a major event in many ocular disorders, including diabetic retinopathy, optic neuropathies and aging-related disorders. The accumulation of damaged mitochondria may pose a severe risk for vision, since 1) damaged mitochondria do not produce energy efficiently and disrupts the power system of the retina and 2) they are a source of toxic waste, which may origin retinal disease. In the healthy retina, this problem is prevented by tight Mitochondrial Quality Control (MQC), where dysfunctional mitochondria are simply removed and replaced by newly-synthetized functional units. Using appropriate in vivo/in vitro experimental models and post-mortem human samples, my research pursues to determine how MQC becomes dysregulated in ocular disease and its contribution to neurovascular degeneration. My main goal focuses in applying this knowledge to develop novel interventional strategies for eye therapy.