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Journal of Ophthalmology
Volume 2014, Article ID 789120, 10 pages
Review Article

Epigenetic Modifications and Potential New Treatment Targets in Diabetic Retinopathy

1EA 7281 R2D2, Medical School, Auvergne University, 63000 Clermont-Ferrand, France
2Department of Biomedicine, University of Aarhus, 8200 Aarhus, Denmark
3Departments of Anatomy/Cell Biology and Ophthalmology, Wayne State University School of Medicine, Detroit, MI 48201, USA

Received 8 April 2014; Revised 22 June 2014; Accepted 17 July 2014; Published 3 August 2014

Academic Editor: Lawrence S. Morse

Copyright © 2014 Lorena Perrone et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Retinopathy is a debilitating vascular complication of diabetes. As with other diabetic complications, diabetic retinopathy (DR) is characterized by the metabolic memory, which has been observed both in DR patients and in DR animal models. Evidences have provided that after a period of poor glucose control insulin or diabetes drug treatment fails to prevent the development and progression of DR even when good glycemic control is reinstituted (glucose normalization), suggesting a metabolic memory phenomenon. Recent studies also underline the role of epigenetic chromatin modifications as mediators of the metabolic memory. Indeed, epigenetic changes may lead to stable modification of gene expression, participating in DR pathogenesis. Moreover, increasing evidences suggest that environmental factors such as chronic hyperglycemia are implicated DR progression and may also affect the epigenetic state. Here we review recent findings demonstrating the key role of epigenetics in the progression of DR. Further elucidation of epigenetic mechanisms, acting both at the cis- and trans-chromatin structural elements, will yield new insights into the pathogenesis of DR and will open the way for the discovery of novel therapeutic targets to prevent DR progression.