Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Diabetic Retinopathy: Mechanistic Insights into High Glucose-Induced Retinal Cell Death

Author(s): Sayon Roy, Kyle Trudeau, Sumon Roy, Thomas Tien, Kevin F. Barrette

Journal Name: Current Clinical Pharmacology
Continued as Current Reviews in Clinical and Experimental Pharmacology

Volume 8 , Issue 4 , 2013


Hyperglycemia, a prominent characteristic of diabetes, has been implicated in the apoptotic death of vascular and neuronal cells in the retina. In diabetic retinopathy, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and subsequent breakdown of cellular homeostasis play a critical role in retinal cell death. In particular, changes in mitochondrial morphology, mitochondrial membrane potential heterogeneity, oxygen consumption rate and protein misfolding are beginning to be recognized as key players in the demise of retinal vascular cells in diabetes. Some of these key changes contribute to oxidative stress and influence ion transport, impacting overall cellular homeostasis. The primary objective of this review is to provide insight into the mechanisms in which high glucose influences two disparate cellular organelles, mitochondria and ER, in promoting apoptotic demise of retinal vascular and neuronal cells in diabetic retinopathy.

Keywords: diabetic retinopathy, ER stress, mitochondria, oxidative stress.

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Article Details

Year: 2013
Published on: 27 September, 2013
Page: [278 - 284]
Pages: 7
DOI: 10.2174/1574884711308040003
Price: $65

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