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ISSN: 2155-9570

Journal of Clinical & Experimental Ophthalmology
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Review Article

Modes of Retinal Cell Death in Diabetic Retinopathy

Derrick J Feenstra1, E. Chepchumba Yego2 and Susanne Mohr1*
1Department of Physiology, Michigan State University, East Lansing, MI, USA
2Research Division, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving, Ground, MD, USA
Corresponding Author : Susanne Mohr, PhD
Michigan State University, Department of Physiology
3175 Biomedical Physical Sciences
East Lansing, MI 44824, USA
Tel: (517) 884-5114
E-mail: [email protected]
Received August 08, 2013; Accepted September 30, 2013; Published October 07, 2013
Citation: Feenstra DJ, Yego EC, Mohr S (2013) Modes of Retinal Cell Death in Diabetic Retinopathy. J Clin Exp Ophthalmol 4:298. doi:10.4172/2155-9570.1000298
Copyright: © 2013 Feenstra DJ, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Cell death seems to be a prominent feature in the progression of diabetic retinopathy. Several retinal cell types have been identified to undergo cell death in a diabetic environment. Most emphasis has been directed towards identifying apoptosis in the diabetic retina. However, new research has established that there are multiple forms of cell death. This review discusses the different modes of cell death and attempts to classify cell death of retinal cells known to die in diabetic retinopathy. Special emphasis is given to apoptosis, necrosis, autophagic cell death, and pyroptosis. It seems that different retinal cell types are dying by diverse types of cell death. Whereas endothelial cells predominantly undergo apoptosis, pericytes might die by apoptosis as well as necrosis. On the other hand, Müller cells are suggested to die by a pyroptotic mechanism. Diabetes leads to significant Müller cell loss at 7 months duration of diabetes in retinas of diabetic mice compared to non-diabetic, which is prevented by the inhibition of the caspase-1/IL-1β (interleukin-1beta) pathway using the IL-1 receptor knockout mouse. Since pyroptosis is characterized by the activation of the caspase-1/IL-1β pathway subsequently leading to cell death, Müller cells seem to be a prime candidate for this form of inflammationdriven cell death. Considering that diabetic retinopathy is now discussed to potentially be a chronic inflammatory disease, pyroptotic cell death might play an important role in disease progression. Understanding mechanisms of cell death will lead to a more targeted approach in the development of new therapies to treat diabetic retinopathy.

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