Advanced Glycation Endproducts and Their Receptor: Do They Play a Role in Diabetic Cardiomyopathy?

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Diabetes mellitus leads to disparate and widespread disease states of the cardiovascular system. Although atherosclerosis of coronary arteries is commonly present in patients with diabetes, an independent phenomenon of heart failure, known as diabetic cardiomyopathy, is the leading cause of death in diabetic patients. Late-stage diabetic cardiomyopathy is characterized by decreased left systolic ventricular pressure, low cardiac output and elevated end-diastolic pressure. However, even in the preclinical stage, impairments in contractionrelaxation performances can be detected. Although altered gene expression has been demonstrated in the diabetic heart, the regulatory mechanism(s) by which this occurs is not clear. The scienti®c progress in exploring these mechanisms has been hampered by the widespread metabolic changes and sheer number of altered molecules in the diabetic state that may contribute to this process. Glucose transported into cells produces metabolites that can interact with multiple intracellular signal transduction pathways. Dysregulation of fatty acid metabolism has been demonstrated in cardiac myocytes from diabetic subjects, and fatty acids may bind with peroxisome proliferator-activated receptors (PPARs) and alter transcription of genes that contain peroxisome

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