Molecular mechanism for accelerated atherosclerosis in diabetes and its potential therapeutic intervention.
Diabetes is associated with a marked increase in the risk of atherosclerotic vascular disorders, including coronary, cerebrovascular and peripheral artery disease. Macrovascular complications could account for disabilities and high mortality rates in patients with diabetes. There is a growing body of evidence to indicate that tight blood glucose control has no more than a marginal impact on cardiovascular disease in diabetes. In this review, we discuss the molecular mechanisms for accelerated atherosclerosis in diabetes and the potential therapeutic interventions, especially focusing on postprandial hyperglycemia and advanced glycation end products (AGEs).
Yamagishi
S
S
Department of Internal Medicine III, Kurume University School of Medicine, Kurume, Japan. shoichi@med.kurume-u.ac.jp
Nakamura
K
K
Takeuchi
M
M
Imaizumi
T
T
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism* / Q000503:physiopathology; D001786:Blood Glucose; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000503:physiopathology; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D006943:Hyperglycemia / Q000378:metabolism / Q000503:physiopathology; D018384:Oxidative Stress; D019518:Postprandial Period
D001786:Blood Glucose; D017127:Glycation End Products, Advanced