Skewed Epigenetics: An Alternative Therapeutic Option for Diabetes Complications
Vascular complications are major causes of morbidity and mortality in type 2 diabetes patients. Mitochondrial reactive oxygen species (ROS) generation and a lack of efficient antioxidant machinery, a result of hyperglycaemia, mainly contribute to this problem. Although advances in therapy have signi...
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Language: | English |
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Wiley
2015-01-01
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Series: | Journal of Diabetes Research |
Online Access: | http://dx.doi.org/10.1155/2015/373708 |
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author | Gabriele Togliatto Patrizia Dentelli Maria Felice Brizzi |
author_facet | Gabriele Togliatto Patrizia Dentelli Maria Felice Brizzi |
author_sort | Gabriele Togliatto |
collection | DOAJ |
description | Vascular complications are major causes of morbidity and mortality in type 2 diabetes patients. Mitochondrial reactive oxygen species (ROS) generation and a lack of efficient antioxidant machinery, a result of hyperglycaemia, mainly contribute to this problem. Although advances in therapy have significantly reduced both morbidity and mortality in diabetic individuals, diabetes-associated vascular complications are still one of the most challenging health problems worldwide. New healing options are urgently needed as current therapeutics are failing to improve long-term outcomes. Particular effort has recently been devoted to understanding the functional relationship between chromatin structure regulation and the persistent change in gene expression which is driven by hyperglycaemia and which accounts for long-lasting diabetic complications. A detailed investigation into epigenetic chromatin modifications in type 2 diabetes is underway. This will be particularly useful in the design of mechanism-based therapeutics which interfere with long-lasting activating epigenetics and improve patient outcomes. We herein provide an overview of the most relevant mechanisms that account for hyperglycaemia-induced changes in chromatin structure; the most relevant mechanism is called “metabolic memory.” |
format | Article |
id | doaj-art-88c512c765ea441394d98d2e420553e6 |
institution | Kabale University |
issn | 2314-6745 2314-6753 |
language | English |
publishDate | 2015-01-01 |
publisher | Wiley |
record_format | Article |
series | Journal of Diabetes Research |
spelling | doaj-art-88c512c765ea441394d98d2e420553e62025-02-03T01:13:14ZengWileyJournal of Diabetes Research2314-67452314-67532015-01-01201510.1155/2015/373708373708Skewed Epigenetics: An Alternative Therapeutic Option for Diabetes ComplicationsGabriele Togliatto0Patrizia Dentelli1Maria Felice Brizzi2Department of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Turin, ItalyDepartment of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Turin, ItalyDepartment of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Turin, ItalyVascular complications are major causes of morbidity and mortality in type 2 diabetes patients. Mitochondrial reactive oxygen species (ROS) generation and a lack of efficient antioxidant machinery, a result of hyperglycaemia, mainly contribute to this problem. Although advances in therapy have significantly reduced both morbidity and mortality in diabetic individuals, diabetes-associated vascular complications are still one of the most challenging health problems worldwide. New healing options are urgently needed as current therapeutics are failing to improve long-term outcomes. Particular effort has recently been devoted to understanding the functional relationship between chromatin structure regulation and the persistent change in gene expression which is driven by hyperglycaemia and which accounts for long-lasting diabetic complications. A detailed investigation into epigenetic chromatin modifications in type 2 diabetes is underway. This will be particularly useful in the design of mechanism-based therapeutics which interfere with long-lasting activating epigenetics and improve patient outcomes. We herein provide an overview of the most relevant mechanisms that account for hyperglycaemia-induced changes in chromatin structure; the most relevant mechanism is called “metabolic memory.”http://dx.doi.org/10.1155/2015/373708 |
spellingShingle | Gabriele Togliatto Patrizia Dentelli Maria Felice Brizzi Skewed Epigenetics: An Alternative Therapeutic Option for Diabetes Complications Journal of Diabetes Research |
title | Skewed Epigenetics: An Alternative Therapeutic Option for Diabetes Complications |
title_full | Skewed Epigenetics: An Alternative Therapeutic Option for Diabetes Complications |
title_fullStr | Skewed Epigenetics: An Alternative Therapeutic Option for Diabetes Complications |
title_full_unstemmed | Skewed Epigenetics: An Alternative Therapeutic Option for Diabetes Complications |
title_short | Skewed Epigenetics: An Alternative Therapeutic Option for Diabetes Complications |
title_sort | skewed epigenetics an alternative therapeutic option for diabetes complications |
url | http://dx.doi.org/10.1155/2015/373708 |
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