Abstract
Diabetic retinopathy is the leading cause of blindness in young adults, and with the incidence of diabetes increasing at a frightening rate, retinopathy is estimated to threaten vision for almost 51 million patients worldwide. In diabetes, mitochondria structure, function and DNA (mtDNA) are damaged in the retina and its vasculature, and the mtDNA repair machinery and biogenesis are compromised. Proteins encoded by mtDNA become subnormal contributing to dysfunctional electron transport system, and the transport of proteins that are important in mtDNA biogenesis and function, but are encoded by nuclear DNA, is impaired. These diabetes-induced abnormalities in mitochondria continue even when hyperglycemic insult is terminated, and are implicated in the metabolic memory phenomenon associated with the continued progression of diabetic retinopathy. Diabetes also facilitates epigenetic modifications-the changes in histones and DNA methylation in response to cells changing environmental stimuli, which the cell can memorize and pass to the next generation. Epigenetic modifications contribute to the mitochondria damage, and are postulated in the development of diabetic retinopathy, and also to the metabolic memory phenomenon. Thus, strategies targeting mitochondria homeostasis and/or enzymes important for histone and DNA methylation could serve as potential therapies to halt the development and progression of diabetic retinopathy.
Keywords: Diabetic retinopathy, epigenetic modifications, mitochondria damage, mitochondria DNA, oxidative stress.
Current Medicinal Chemistry
Title:Mitochondria Damage in the Pathogenesis of Diabetic Retinopathy and in the Metabolic Memory Associated with its Continued Progression
Volume: 20 Issue: 26
Author(s): Renu A. Kowluru
Affiliation:
Keywords: Diabetic retinopathy, epigenetic modifications, mitochondria damage, mitochondria DNA, oxidative stress.
Abstract: Diabetic retinopathy is the leading cause of blindness in young adults, and with the incidence of diabetes increasing at a frightening rate, retinopathy is estimated to threaten vision for almost 51 million patients worldwide. In diabetes, mitochondria structure, function and DNA (mtDNA) are damaged in the retina and its vasculature, and the mtDNA repair machinery and biogenesis are compromised. Proteins encoded by mtDNA become subnormal contributing to dysfunctional electron transport system, and the transport of proteins that are important in mtDNA biogenesis and function, but are encoded by nuclear DNA, is impaired. These diabetes-induced abnormalities in mitochondria continue even when hyperglycemic insult is terminated, and are implicated in the metabolic memory phenomenon associated with the continued progression of diabetic retinopathy. Diabetes also facilitates epigenetic modifications-the changes in histones and DNA methylation in response to cells changing environmental stimuli, which the cell can memorize and pass to the next generation. Epigenetic modifications contribute to the mitochondria damage, and are postulated in the development of diabetic retinopathy, and also to the metabolic memory phenomenon. Thus, strategies targeting mitochondria homeostasis and/or enzymes important for histone and DNA methylation could serve as potential therapies to halt the development and progression of diabetic retinopathy.
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Cite this article as:
Kowluru A. Renu, Mitochondria Damage in the Pathogenesis of Diabetic Retinopathy and in the Metabolic Memory Associated with its Continued Progression, Current Medicinal Chemistry 2013; 20 (26) . https://dx.doi.org/10.2174/09298673113209990029
DOI https://dx.doi.org/10.2174/09298673113209990029 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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