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Diabetic photoreceptors: Mechanisms underlying changes in structure and function

Published online by Cambridge University Press:  06 October 2020

Silke Becker
Affiliation:
John A. Moran Eye Center, University of Utah, Salt Lake City, Utah
Lara S. Carroll
Affiliation:
John A. Moran Eye Center, University of Utah, Salt Lake City, Utah
Frans Vinberg*
Affiliation:
John A. Moran Eye Center, University of Utah, Salt Lake City, Utah
*
Address correspondence to: Frans Vinberg, E-mail: frans.vinberg@utah.edu

Abstract

Based on clinical findings, diabetic retinopathy (DR) has traditionally been defined as a retinal microvasculopathy. Retinal neuronal dysfunction is now recognized as an early event in the diabetic retina before development of overt DR. While detrimental effects of diabetes on the survival and function of inner retinal cells, such as retinal ganglion cells and amacrine cells, are widely recognized, evidence that photoreceptors in the outer retina undergo early alterations in diabetes has emerged more recently. We review data from preclinical and clinical studies demonstrating a conserved reduction of electrophysiological function in diabetic retinas, as well as evidence for photoreceptor loss. Complementing in vivo studies, we discuss the ex vivo electroretinography technique as a useful method to investigate photoreceptor function in isolated retinas from diabetic animal models. Finally, we consider the possibility that early photoreceptor pathology contributes to the progression of DR, and discuss possible mechanisms of photoreceptor damage in the diabetic retina, such as enhanced production of reactive oxygen species and other inflammatory factors whose detrimental effects may be augmented by phototransduction.

Type
Review Article
Copyright
© The Author(s), 2020. Published by Cambridge University Press

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Footnotes

Silke Becker and Lara S. Carroll contributed equally to this study.

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