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Advanced glycation end products in diabetes-associated atherosclerosis and renal disease: interventional studies
Karin A Jandeleit-Dahm1, Markus Lassila, Terri J Allen
1Danielle Alberti Memorial Centre for Diabetes Complications, Baker Heart Research Institute, P.O. Box 6492, Melbourne 8008, Australia.
Abstract:
There is increasing evidence that advanced glycation end products (AGEs) and their interactions with various receptors (in particular, the receptor RAGE) play a pivotal role in the development and progression of diabetic macro- and microvascular complications. Several approaches have been used to inhibit tissue accumulation of AGEs in diabetes, including inhibitors of AGE formation such as aminoguanidine, ALT 946, and pyridoxamine-or putative cross-link breakers such as ALT 711. Alternative interventions have also included the administration of a soluble receptor for RAGE, sRAGE, thus capturing circulating AGEs and preventing them from binding to the cell-bound full-length receptor RAGE, thereby inhibiting the proinflammatory and profibrotic response following AGE-RAGE binding. In this review we summarize the evidence for such antiglycation therapies in retarding or delaying the development and progression of diabetes-associated atherosclerosis and renal disease while focusing on interventional strategies inhibiting AGE accumulation. In summary, all approaches have been shown to confer some degree of antiatherosclerotic and renoprotective effects, albeit to different degrees and by different mechanisms.
Insights
Advanced glycation end products (AGEs) contribute to diabetic vascular complications. Antiglycation therapies show promise in delaying atherosclerosis and renal disease by inhibiting AGE accumulation.
Area of Science:
- Endocrinology and Metabolism
- Vascular Biology
- Nephrology
Background:
- Advanced glycation end products (AGEs) are implicated in diabetic vascular complications.
- The receptor for AGEs (RAGE) mediates AGE-induced inflammation and fibrosis.
- Diabetic macro- and microvascular complications are linked to AGE-RAGE interactions.
Purpose of the Study:
- To review antiglycation therapies for diabetic complications.
- To focus on interventions inhibiting AGE accumulation.
- To evaluate therapeutic strategies targeting the AGE-RAGE axis.
Main Methods:
- Review of studies on AGE formation inhibitors (e.g., aminoguanidine, pyridoxamine).
- Analysis of cross-link breakers (e.g., ALT 711).
- Evaluation of soluble RAGE (sRAGE) as a therapeutic intervention.
Main Results:
- Inhibitors of AGE formation demonstrated renoprotective and antiatherosclerotic effects.
- Cross-link breakers showed potential in mitigating AGE-related damage.
- sRAGE administration captured circulating AGEs, reducing RAGE-mediated responses.
- All reviewed approaches conferred some degree of protection against atherosclerosis and renal disease.
Conclusions:
- Antiglycation therapies represent a viable strategy for managing diabetic vascular complications.
- Targeting AGE accumulation and RAGE signaling offers therapeutic benefits.
- Further research is warranted to optimize these interventions for clinical application.
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