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Nonenzymatic glycosylation of macromolecules. Prospects of pharmacologic modulation
1Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461.
Insights
Diabetes elevates atherosclerotic arterial disease risk. Chronic hyperglycemia may accelerate this process via arterial wall glycation, a mechanism explored with the potential inhibitor aminoguanidine.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Biochemistry
Background:
- Diabetes mellitus significantly elevates the risk of atherosclerotic arterial disease.
- Hyperglycemia is a known risk factor, but its relationship with macrovascular complications is complex due to multifactorial influences on atherogenesis.
- In vitro studies suggest chronic hyperglycemia accelerates atherosclerosis through excessive glycation of arterial wall components.
Purpose of the Study:
- To critically review the relationship between hyperglycemia and atherosclerotic arterial disease.
- To discuss the biochemical mechanisms by which chronic hyperglycemia may promote atherogenesis.
- To explore the pharmacological potential of aminoguanidine as a glycation inhibitor.
Main Methods:
- Literature review of studies investigating hyperglycemia and atherosclerosis.
- Critical analysis of in vitro data on arterial wall glycation.
- Biochemical review of glycation pathways and aminoguanidine's mechanism of action.
Main Results:
- Elevated glycohemoglobin is an independent risk factor for macrovascular disease in specific populations.
- Chronic hyperglycemia appears to accelerate the atherogenic process via excessive glycation of arterial wall constituents.
- Aminoguanidine exhibits potential as a pharmacological inhibitor of glycation.
Conclusions:
- Hyperglycemia is a significant contributor to accelerated atherosclerosis, primarily through glycation pathways.
- Aminoguanidine presents a potential therapeutic strategy for mitigating diabetic macrovascular complications by inhibiting glycation.
Abstract:
Diabetes increases the risk of developing atherosclerotic arterial disease significantly. Although elevated glycohemoglobin was shown to be an independent risk factor in older women in the Framingham Heart Study, the relationship between hyperglycemia and macrovascular disease is complicated by the many other factors that influence atherogenesis in nondiabetic people. Studies in vitro suggest that chronic hyperglycemia may accelerate the atherogenic process through excessive glycation of various components of the arterial wall. These data are reviewed critically, and the biochemistry and pharmacological potential of the glycation-inhibitor aminoguanidine is discussed.