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Pigment Epithelium-derived Factor Inhibits Advanced Glycation End Product-induced Retinal Vascular Hyperpermeability by Blocking Reactive Oxygen Species- mediated Vascular Endothelial Growth Factor Expression *

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TLDR
Results indicate that the central mechanism for PEDF inhibition of the AGE signaling to vascular permeability is by suppression of NADPH oxidase-mediated ROS generation and subsequent VEGF expression, which may offer a promising strategy for halting the development of diabetic retinopathy.
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This article is published in Journal of Biological Chemistry.The article was published on 2006-07-21 and is currently open access. It has received 198 citations till now. The article focuses on the topics: PEDF & Vascular endothelial growth factor B.

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Vascular endothelial growth factor in eye disease.

TL;DR: The roles played by VEGF in the pathogenesis of retinopathy of prematurity, diabetic Retinopathy and age-related macular degeneration are described and the potential disadvantages of inhibiting VEGf will be discussed, as will the rationales for targeting other V EGF-related modulators of angiogenesis.
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Advanced glycation end products, oxidative stress and diabetic nephropathy.

TL;DR: The pathophysiological role of AGEs and their receptor (RAGE)-oxidative stress system in diabetic nephropathy is reviewed and accumulating evidence that advanced glycation end products (AGEs), senescent macroprotein derivatives formed at an accelerated rate under diabetes, play a role in diabetes via oxidative stress generation.
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The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality.

TL;DR: It is shown how invertebrate models, notably Drosophila melanogaster and Caenorhabditis elegans, can be used to explore AGE-related pathways in depth and to identify and assess drugs that will mitigate against the detrimental effects of AGEs-adduct development.
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Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications.

TL;DR: The abnormalities correlated with oxidative stress provide multiple potential therapeutic targets to develop safe and effective treatments for diabetic retinopathy and are summarized.
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Role of advanced glycation end products (AGEs) and oxidative stress in vascular complications in diabetes.

TL;DR: Observations suggest that inhibition of AGE-RAGE-oxidative stress axis or blockade of its interaction with RAS is a novel therapeutic strategy for preventing vascular complications in diabetes.
References
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Journal ArticleDOI

The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus.

TL;DR: Intensive therapy effectively delays the onset and slows the progression of diabetic retinopathy, nephropathy, and neuropathy in patients with IDDM.
Journal Article

Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)

R C Turner, +398 more
- 12 Sep 1998 - 
TL;DR: In this article, the effects of intensive blood-glucose control with either sulphonylurea or insulin and conventional treatment on the risk of microvascular and macrovascular complications in patients with type 2 diabetes in a randomised controlled trial were compared.
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Biochemistry and molecular cell biology of diabetic complications

TL;DR: This integrating paradigm provides a new conceptual framework for future research and drug discovery in diabetes-specific microvascular disease and seems to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain.

superoxide production blocks three pathways of hyperglycaemic damage

TL;DR: This paper showed that hyperglycaemia increases the production of reactive oxygen species inside cultured bovine aortic endothelial cells and that this increase in reactive oxygen can be prevented by an inhibitor of electron transport chain complex II, an uncoupler of oxidative phosphorylation, by uncoupling protein-1 and by manganese superoxide dismutase.
Journal ArticleDOI

Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage

TL;DR: This work shows that hyperglycaemia increases the production of reactive oxygen species inside cultured bovine aortic endothelial cells and is prevented by an inhibitor of electron transport chain complex II, by an uncoupler of oxidative phosphorylation, by uncoupling protein-1 and by manganese superoxide dismutase.
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