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Updated: Aug 9, 2026

Isolation of Intermediate Filament Proteins from Multiple Mouse Tissues to Study Aging-associated Post-translational Modifications
Published on: May 18, 2017
[Advanced glycosylation end products (AGE): new toxins?]
E Boulanger1, Ph Dequiedt, J L Wautier
1Laboratoire de recherche en biologie vasculaire et cellulaire, INTS, Paris. eboulanger@ints.fr
Abstract:
Advanced glycation end-products (AGEs) are found in excess during diabetes mellitus, uremia and aging. Non enzymatique glycation, glycoxidation with glucose auto-oxidation and the polyol pathway are involved in the production of AGEs. Tissue accumulation of AGEs and their binding to cell receptors are critical steps in the deleterious consequences of AGE excess. AGE-receptor interaction altered endothelial cells, macrophages, mesangial and mesothelial cell functions. AGEs appear to be involved in the genesis of diabetic micro but also macro-angiopathy. Reduction of AGE clearance and permanent oxidative stress are responsible for AGE excess during uremia. High-flux hemodialysis and peritoneal dialysis reduce AGE level but kidney transplantation is the best treatment to restore homeostasis. New drugs are tested to reduce AGEs or AGE deleterious effects but the best treatment remains the prevention of AGE formation by a strict glycemic control.
Insights
Advanced glycation end-products (AGEs) accumulate in diabetes, uremia, and aging, contributing to cellular dysfunction and vascular complications. Managing AGEs through glycemic control and transplantation is key to preventing their harmful effects.
Area of Science:
- Biochemistry
- Pathophysiology
- Endocrinology
Background:
- Advanced glycation end-products (AGEs) accumulate in conditions like diabetes mellitus, uremia, and aging.
- AGEs are formed through non-enzymatic glycation, glycoxidation, and the polyol pathway.
- Tissue accumulation and receptor binding of AGEs contribute to cellular dysfunction and disease pathogenesis.
Purpose of the Study:
- To review the role of AGEs in pathological conditions.
- To discuss the mechanisms of AGE formation and accumulation.
- To evaluate current and potential therapeutic strategies for managing AGEs.
Main Methods:
- Literature review of AGEs' role in diabetes, uremia, and aging.
- Analysis of AGEs' impact on cellular functions and vascular complications.
- Evaluation of therapeutic interventions, including dialysis, transplantation, and pharmacologic approaches.
Main Results:
- AGE accumulation is linked to endothelial, macrophage, mesangial, and mesothelial cell dysfunction.
- AGEs are implicated in the development of diabetic micro- and macro-angiopathy.
- While dialysis can reduce AGE levels, kidney transplantation is most effective in restoring homeostasis; strict glycemic control remains crucial for prevention.
Conclusions:
- AGEs play a significant role in the deleterious consequences of diabetes, uremia, and aging.
- Effective management strategies include reducing AGE formation and enhancing their clearance.
- Prevention through strict glycemic control is the most effective long-term strategy against AGE-related complications.
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