Role of retinal mitochondria in the development of diabetic retinopathy

Abstract

Diabetic retinopathy is the leading cause of acquired blindness in developed countries. Prolonged hyperglycemia precipitates the oxidative stress that mediates mitochondrial dysfunctions associated with diabetic retinopathy. Mitochondrial reactive oxygen species are elevated in diabetic retina damaging the mitochondrial macromolecules. Membrane injury increases mitochondrial permeability driving Bax translocation into and cytochrome-c release out of the mitochondria, activating caspases and thus, apoptosis of the retinal capillary endothelial cells and pericytes. Antioxidants and superoxide dismutase mimics have shown potential in the inhibition of diabetes-induced oxidative stress, capillary cell apoptosis and histopathology characteristic of diabetic retinopathy, and overexpression of manganese superoxide dismutase in mice provides protection from diabetes-induced abnormalities in the retinal mitochondria. Elucidating the role of mitochondrial dysfunctions in diabetic retinopathy is essential to the development of mitochondria-targeted treatments for this disease.

Keywords::

• antioxidants
• diabetic retinopathy
• mitochondrial dysfunction
• oxidative stress
• retina
• superoxide dismutase