Targeting epigenetic modifications as a potential therapeutic option for diabetic retinopathy

Diabetic retinopathy (DR) is the leading cause of visual impairment in adults of working age (20–65 years) in developed countries. The metabolic memory phenomena (persistent effect of a glycemic insult even after retrieved) associated with it has increased the risk of developing the complication eve...

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Veröffentlicht in:Journal of cellular physiology 2020-03, Vol.235 (3), p.1933-1947
Hauptverfasser: Kumari, Nidhi, Karmakar, Aditi, Ganesan, Senthil kumar
Format: Artikel
Sprache:eng
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Zusammenfassung:Diabetic retinopathy (DR) is the leading cause of visual impairment in adults of working age (20–65 years) in developed countries. The metabolic memory phenomena (persistent effect of a glycemic insult even after retrieved) associated with it has increased the risk of developing the complication even after the termination of the glycemic insult. Hence, the need for finding early diagnosis and treatment options has been of great concern. Epigenetic modifications which generally occur during the beginning stages of the disease are responsible for the metabolic memory effect. Therefore, the therapy based on the reversal of the associated epigenetic mechanism can bring new insight in the area of early diagnosis and treatment mechanism. This review discusses the diabetic retinopathy, its pathogenesis, current treatment options, need of finding novel treatment options, and different epigenetic alterations associated with DR. However, the main focus is emphasized on various epigenetic modifications particularly DNA methylation which are responsible for the initiation and progression of diabetic retinopathy and the use of different epigenetic inhibitors as a novel therapeutic option for DR. This review article essentially discusses various epigenetic modifications which are responsible for the initiation and progression of diabetic retinopathy (DR) and demand for epigenetic therapies for DR management.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.29180