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[Aging: role and control of glycation]
E Boulanger1, F Puisieux, C Gaxatte
1Biologie du vieillissement vasculaire, pôle de recherche, faculté de médecine, CHRU de Lille-II, 1, place de Verdun, 59045 Lille, France. eboulanger@chru-lille.fr
La Revue De Medecine Interne
|June 29, 2007
Summary
Advanced glycation end-products (AGEs) are aging toxins implicated in diseases like diabetes and Alzheimer's. Inhibiting AGE formation or their receptor interactions shows promise in preventing AGE-related cellular damage.
Area of Science:
- Biochemistry
- Pathophysiology
- Aging Research
Background:
- Advanced glycation end-products (AGEs) form via non-enzymatic glycation and glycoxidation.
- AGEs accumulate in aging tissues and are implicated in diseases like diabetes, rheumatoid arthritis, and Alzheimer's.
- AGEs exert toxicity through receptor binding (e.g., RAGE) and accumulation of glycated proteins.
Purpose of the Study:
- To explore the role of AGEs in cellular alteration and organ dysfunction.
- To understand the mechanisms of AGE toxicity, including endothelial dysfunction.
- To highlight the significance of AGE-receptor interactions in disease pathogenesis.
Main Methods:
- Review of in vitro and animal studies.
- Analysis of pathophysiological mechanisms of AGE toxicity.
- Examination of AGE formation pathways.
Main Results:
- AGEs contribute to endothelial dysfunction and macro/micro-angiopathy in diabetes.
- AGE-receptor activation triggers pro-inflammatory, pro-coagulant, and pro-fibrotic responses.
- AGEs cause cell and organ damage through receptor binding and protein accumulation.
Conclusions:
- In vitro and animal studies suggest AGE deleterious effects can be prevented.
- Strategies include glycation inhibitors, AGE cross-link breakers, and AGE-RAGE interaction inhibition.
- New molecules are under investigation for preventing or treating AGE-related damage.
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