Advanced glycation end products and vascular structure and function.
Diabetes mellitus has now reached epidemic proportions in the Western world. The associated microvascular and macrovascular complications are a result of severe metabolic derangement, which leads to chronic tissue injury. Although there are a number of proposed pathophysiologic mechanisms for the vascular complications associated with diabetes, this review focuses predominantly on the role of advanced glycation end products (AGEs) in the pathogenesis of diabetes-associated atherosclerosis. The potential role of AGEs in enhancing arterial stiffness, an entity occurring with a greater prevalence in populations known to have higher-than-normal AGE levels, is also examined. Pharmacologic interventions aimed at reducing the level of these chemical compounds or interrupting their action provide hope for the future treatment of both atherosclerotic vascular disease and systolic hypertension, particularly in the setting of diabetes.
Soldatos
Georgia
G
Baker Medical Research Institute, Melbourne, Victoria 8008, Australia. Georgia.Soldatos@baker.edu.au
Cooper
Mark Emmanuel
ME
D000818:Animals; D050197:Atherosclerosis / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D017127:Glycation End Products, Advanced / Q000502:physiology*; D006801:Humans; D008213:Lymphocyte Activation / Q000502:physiology; D000067759:Receptor for Advanced Glycation End Products / Q000502:physiology*; D013844:Thiazoles / Q000378:metabolism
C000593871:AGER protein, human; D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D013844:Thiazoles; C406794:alagebrium