Diabetes Induces Accumulation of Carbonylated Proteins in the Rat Retinal Pigment Epithelium Independently of Oxidative Stress.

ABSTRACT: Diabetic retinopathy (DR) is a major complication of diabetes mellitus. Growing evidence shows that hyperglycemia causes not only microvascular damage but also retinal neural dysfunction. Although different metabolic pathways have been implicated, the exact mechanism behind retinal degeneration remains unclear. Hyperglycemic stimuli have been shown to reduce the function of the retinal blood-barrier (BRB) in both diabetic humans and animals. As part of the BRB, the retinal pigment epithelium (RPE) plays a key role in retinal function by regulating the flow of metabolites and ions between the choroidal blood supply and the outer retina, and by supporting photoreceptor cell functions. Therefore, RPE dysfunction can lead to retinal injury. To understand the role of RPE in DR, we studied oxida

SUBMITTER: Morales-Ramirez E 

PROVIDER: S-EPMC12824452 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature