Abstract
As is diabetes itself, diabetic angiopathy is a multi-factorial disease. Advanced glycation endproducts (AGE) cause vascular cell derangement characteristic of diabetes, and this is mainly mediated by their interaction with receptor for AGE (RAGE). When made diabetic, RAGE-overexpressing transgenic mice exhibited exacerbation of the indices of nephropathy, and this was prevented by the inhibition of AGE formation. On the other hand, RAGE-deficient animals showed amelioration of diabetic nephropathy. Accordingly, AGE and RAGE should be regarded as environmental and cellular accounts and as a potential therapeutic target for diabetic nephropathy. In effect, substances that inhibit the formation of AGE, break preformed AGE, change metabolic flows away from glycation, antagonize RAGE, and capture RAGE ligands have been proven as effective remedies against this life-threatening disease.
Keywords: iNOS transgenic mice, endothelial cells, aminoguanidine, RAGE gene, diabetic nephropathy
Current Molecular Medicine
Title: RAGE in Diabetic Nephropathy
Volume: 7 Issue: 8
Author(s): Hiroshi Yamamoto, Takuo Watanabe, Yasuhiko Yamamoto, Hideto Yonekura, Seiichi Munesue, Ai Harashima, Kazuyo Ooe, Sharmin Hossain, Hidehito Saito and Naho Murakami
Affiliation:
Keywords: iNOS transgenic mice, endothelial cells, aminoguanidine, RAGE gene, diabetic nephropathy
Abstract: As is diabetes itself, diabetic angiopathy is a multi-factorial disease. Advanced glycation endproducts (AGE) cause vascular cell derangement characteristic of diabetes, and this is mainly mediated by their interaction with receptor for AGE (RAGE). When made diabetic, RAGE-overexpressing transgenic mice exhibited exacerbation of the indices of nephropathy, and this was prevented by the inhibition of AGE formation. On the other hand, RAGE-deficient animals showed amelioration of diabetic nephropathy. Accordingly, AGE and RAGE should be regarded as environmental and cellular accounts and as a potential therapeutic target for diabetic nephropathy. In effect, substances that inhibit the formation of AGE, break preformed AGE, change metabolic flows away from glycation, antagonize RAGE, and capture RAGE ligands have been proven as effective remedies against this life-threatening disease.
Export Options
About this article
Cite this article as:
Yamamoto Hiroshi, Watanabe Takuo, Yamamoto Yasuhiko, Yonekura Hideto, Munesue Seiichi, Harashima Ai, Ooe Kazuyo, Hossain Sharmin, Saito Hidehito and Murakami Naho, RAGE in Diabetic Nephropathy, Current Molecular Medicine 2007; 7 (8) . https://dx.doi.org/10.2174/156652407783220769
DOI https://dx.doi.org/10.2174/156652407783220769 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Current Concepts in Gastric Motility in Diabetes Mellitus
Current Diabetes Reviews Dysregulation of Neurotrophic and Haematopoietic Growth Factors in Alzheimer’s Disease: From Pathophysiology to Novel Treatment Strategies
Current Alzheimer Research Small Molecule Fluorescent Probes for the Detection of Amyloid Self-Assembly In Vitro and In Vivo
Current Protein & Peptide Science Haptoglobin Phenotype Correlates with the Extent of Cerebral Deep White Matter Lesions in Hypertensive Patients
Current Neurovascular Research Patent Selections
Recent Patents on Endocrine, Metabolic & Immune Drug Discovery Intracranial MR Dynamics in Clinically Diagnosed Alzheimers Disease: The Emerging Concept of “Pulse Wave Encephalopathy”
Current Alzheimer Research Incretins and Preservation of Endothelial Function
Cardiovascular & Hematological Agents in Medicinal Chemistry Management of Dyslipidaemia for the Prevention of Stroke: Clinical Practice Recommendations from the Lipid Association of India
Current Vascular Pharmacology Regulation of Matrix Synthesis, Remodeling and Accumulation in Glomerulosclerosis
Current Pharmaceutical Design Diabetes and Vascular Disease: Basic Concepts of Nitric Oxide Physiology, Endothelial Dysfunction, Oxidative Stress and Therapeutic Possibilities
Current Vascular Pharmacology Consequences of Aberrant Insulin Regulation in the Brain: Can Treating Diabetes be Effective for Alzheimers Disease
Current Neuropharmacology Insight to the Pathophysiology of Stable Angina Pectoris
Current Pharmaceutical Design Therapeutic Approach on AGE-RAGE Interaction and Its Function in Diabetic Inflammation Process
Recent Patents on Endocrine, Metabolic & Immune Drug Discovery Long-Term Effects of Intracerebroventricular Streptozotocin Treatment on Adult Neurogenesis in the Rat Hippocampus
Current Alzheimer Research Cellular and Molecular Mechanisms of Dementia: Decoding the Causal link of Diabetes Mellitus in Alzheimer’s Disease
CNS & Neurological Disorders - Drug Targets G-Lymphatic, Vascular and Immune Pathways for Aβ Clearance Cascade and Therapeutic Targets For Alzheimer’s Disease
Combinatorial Chemistry & High Throughput Screening Anti-Diabetic Effects of Isolated Lipids from Natural Sources through Modulation of Angiogenesis
Current Molecular Pharmacology Aminoacid Support in the Prevention of Diabetes and Diabetic Complications
Current Protein & Peptide Science GSK-3 Inhibitors: A New Class of Drugs for Alzheimer’s Disease Treatment
Current Drug Targets Abnormalities of Peptide Metabolism in Alzheimer Disease
Current Neurovascular Research