Receptor for advanced glycation end products and the cardiovascular complications of diabetes and beyond: lessons from AGEing.
The presence of elevated blood glucose levels characterizes the diabetic state. Hyperglycemia may be caused by a number of underlying factors; however, the consequences of chronically elevated glucose are similar. Both the macrovasculature and microvasculature are exquisitely sensitive to the long-term effects of elevated blood glucose. Cardiovascular disease remains the leading cause of morbidity and mortality in diabetes, regardless of the underlying cause of hyperglycemia. Although other substrates, such as DNA, are susceptible to glycation, this article addresses the impact of nonenzymatic glycation on the proteome. The impact of Advanced Glycation End products (AGEs) on alteration of protein function and signal transduction mechanisms contributes to the pathogenesis of diabetes complications. This suggests that blocking the generation or molecular impact of AGEs may modulate the complications of diabetes.
Yan
Shi Fang
SF
Columbia University Medical Center, 630 West 168th Street, P&S 17-501, New York, NY 10032, USA.
Yan
Shi Du
SD
Herold
Kevan
K
Ramsamy
Ravichandran
R
Schmidt
Ann Marie
AM
D000818:Animals; D050197:Atherosclerosis; D002318:Cardiovascular Diseases / Q000209:etiology*; D023903:Coronary Restenosis; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000209:etiology / Q000628:therapy; D004195:Disease Models, Animal; D017127:Glycation End Products, Advanced; D006801:Humans; D007249:Inflammation / Q000150:complications; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic
D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic