Journal
CURRENT CLINICAL PHARMACOLOGY
Volume 8, Issue 4, Pages 278-284Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1574884711308040003
Keywords
diabetic retinopathy; ER stress; mitochondria; oxidative stress
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Funding
- NEI
- Boston University Undergraduate Research Opportunities Program
- Boston University MSSR Program
- NIH [EY018218]
- Massachusetts Lions Organization
- NATIONAL EYE INSTITUTE [R01EY018218] Funding Source: NIH RePORTER
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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.
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