alexa Thioredoxin Interacting Protein (TXNIP) and Pathogenesis of Diabetic Retinopathy
ISSN: 2155-9570

Journal of Clinical & Experimental Ophthalmology
Open Access

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Review Article

Thioredoxin Interacting Protein (TXNIP) and Pathogenesis of Diabetic Retinopathy

Lalit P Singh*, Lorena Perrone
Departments of Anatomy and Cell Biology and Ophthalmology, Wayne State University School of Medicine, Detroit, MI 48201, USA
Corresponding Author : Lalit P Singh, Ph.D.
Departments of Anatomy and Cell Biology and Ophthalmology
Wayne State University School of Medicine
540 E Canfield, Scott Hall 8332
Detroit, MI 48201, USA
Tel: 313-577-5032
E-mail: [email protected]
Received June 06, 2013; Accepted July 31, 2013; Published August 05, 2013
Citation: Singh LP, Perrone L (2013) Thioredoxin Interacting Protein (TXNIP) and Pathogenesis of Diabetic Retinopathy. J Clin Exp Ophthalmol 4:287. doi: 10.4172/2155-9570.1000287
Copyright: © 2013 Singh LP, 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

Chronic hyperglycemia (HG)-associated reactive oxygen/nitrogen species (ROS/RNS) stress and low grade inflammation are considered to play critical roles in the development of diabetic retinopathy (DR). Excess glucose metabolic flux through the aldose reductase/polyol pathway, advanced glycation end product (AGE) formation, elevated hexosamine biosynthesis pathway (HBP), diacyl glycerol/PKC activation, and mitochondrial ROS generation are all implicated in DR. In addition, endoplasmic reticulum stress/unfolded protein response (er-UPR) and deregulation of mitochondrial quality control by autophagy/mitophagy are observed causing cellular bioenergetic deficiency and injury. Recently, a pro-oxidant and pro-apoptotic thioredoxin interacting protein (TXNIP) was shown to be highly up-regulated in DR and by HG in retinal cells in culture. TXNIP binds to thioredoxin (Trx) inhibiting its oxidant scavenging and thiolreducing capacity. Hence, prolonged overexpression of TXNIP causes ROS/RNS stress, mitochondrial dysfunction, inflammation and premature cell death in DR. Initially, DR was considered as microvascular complications of endothelial dysfunction and pericyte loss characterized by capillary basement membrane thickening, pericyte ghost, blood retinal barrier leakage, acellular capillary and neovascularization. However, it is currently acknowledged that neuro-glia are also affected by HG in diabetes and that neuronal injury, glial activation, innate immunity/sterile inflammation, and ganglion apoptosis occur early in DR. In addition, retinal pigment epithelium (RPE) becomes dysfunctional in DR. Since TXNIP is induced by HG in most cells, its effects are not restricted to a particular cell type in DR. However, depending on the metabolic activity and anti-oxidant capacity, some cells may be affected earlier by TXNIP than others. Identification of TXNIP sensitive cells and elucidating the underlying mechanism(s) will be critical for preventing pre-mature cell death and progression of DR.

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