Glycoxidation, a relatively slow process in vivo, is a common mechanism for the generation of Advanced Glycation Endproducts (AGEs). However, diabetes in conjunction with uremia is the major source of AGEs. The accumulation of AGEs is more important in proteins with long half-lives, such as collagen or lens protein crystallin. However the impact of AGEs accumulation is important in almost all body tissues, as it contributes to structural modifications and functional impairment. Moreover, the interaction of AGEs with their related receptor, stimulates a series of cellular responses including the release of free radicals, activation of the NFkB cascade and MAP kinases. These cellular responses play a role in the onset and development of late diabetic complications such as micro-, macro-angiopathy, and neuropathy. The cellular damage of diabetic pathophysiology is not just a result of endogenous AGEs production. Studies have shown that AGEs induced by dietary or smoking factors (i.e. glycotoxins) are also involved. Further studies of the glycoxidative cascade have lead to the identification and development of several potential inhibitors of this pathway.
Glycoxidation and diabetic complications; from benchmark to clinical field
ODETTI, PATRIZIO;MONACELLI, FIAMMETTA
2010-01-01
Abstract
Glycoxidation, a relatively slow process in vivo, is a common mechanism for the generation of Advanced Glycation Endproducts (AGEs). However, diabetes in conjunction with uremia is the major source of AGEs. The accumulation of AGEs is more important in proteins with long half-lives, such as collagen or lens protein crystallin. However the impact of AGEs accumulation is important in almost all body tissues, as it contributes to structural modifications and functional impairment. Moreover, the interaction of AGEs with their related receptor, stimulates a series of cellular responses including the release of free radicals, activation of the NFkB cascade and MAP kinases. These cellular responses play a role in the onset and development of late diabetic complications such as micro-, macro-angiopathy, and neuropathy. The cellular damage of diabetic pathophysiology is not just a result of endogenous AGEs production. Studies have shown that AGEs induced by dietary or smoking factors (i.e. glycotoxins) are also involved. Further studies of the glycoxidative cascade have lead to the identification and development of several potential inhibitors of this pathway.
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