Abstract
Diabetic vascular complication is a leading cause of acquired blindness, end-stage renal failure, a variety of neuropathies and accelerated atherosclerosis, which could account for disabilities and high mortality rates in patients with diabetes. Although several hyperglycemia- elicited metabolic and hemodynamic derangements have been implicated in the pathogenesis of diabetic vascular complication, the process of formation and accumulation of advanced glycation end products (AGEs) and their mode of action are most compatible with the theory ‘hyperglycemic memory’. Further, there is a growing body of evidence that AGEs and their receptor (RAGE) axis is involved in the pathogenesis of diabetic vascular complication. Indeed, the engagement of RAGE with AGEs is shown to elicit oxidative stress generation and subsequently evoke inflammatory responses in various types of cells, thus playing an important role in the development and progression of diabetic micro- and macroangiopathy. These observations suggest that down-regulation of RAGE expression or blockade of the RAGE downstream signaling may be a promising target for therapeutic intervention in diabetic vascular complication. In this review, we discuss several types of agents that could potentially inhibit RAGE expression or its downstream pathways and their therapeutic implications in diabetic vascular complication.
Keywords: Diabetic vascular complication, AGEs, oxidative stress, RAGE
Current Pharmaceutical Design
Title: Receptor for Advanced Glycation End Products (RAGE): A Novel Therapeutic Target for Diabetic Vascular Complication
Volume: 14 Issue: 5
Author(s): Sho-ichi Yamagishi, Kazuo Nakamura, Takanori Matsui, Yoshihiro Noda and Tsutomu Imaizumi
Affiliation:
Keywords: Diabetic vascular complication, AGEs, oxidative stress, RAGE
Abstract: Diabetic vascular complication is a leading cause of acquired blindness, end-stage renal failure, a variety of neuropathies and accelerated atherosclerosis, which could account for disabilities and high mortality rates in patients with diabetes. Although several hyperglycemia- elicited metabolic and hemodynamic derangements have been implicated in the pathogenesis of diabetic vascular complication, the process of formation and accumulation of advanced glycation end products (AGEs) and their mode of action are most compatible with the theory ‘hyperglycemic memory’. Further, there is a growing body of evidence that AGEs and their receptor (RAGE) axis is involved in the pathogenesis of diabetic vascular complication. Indeed, the engagement of RAGE with AGEs is shown to elicit oxidative stress generation and subsequently evoke inflammatory responses in various types of cells, thus playing an important role in the development and progression of diabetic micro- and macroangiopathy. These observations suggest that down-regulation of RAGE expression or blockade of the RAGE downstream signaling may be a promising target for therapeutic intervention in diabetic vascular complication. In this review, we discuss several types of agents that could potentially inhibit RAGE expression or its downstream pathways and their therapeutic implications in diabetic vascular complication.
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Cite this article as:
Yamagishi Sho-ichi, Nakamura Kazuo, Matsui Takanori, Noda Yoshihiro and Imaizumi Tsutomu, Receptor for Advanced Glycation End Products (RAGE): A Novel Therapeutic Target for Diabetic Vascular Complication, Current Pharmaceutical Design 2008; 14 (5) . https://dx.doi.org/10.2174/138161208783597416
DOI https://dx.doi.org/10.2174/138161208783597416 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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