The formation of advanced glycation end-products(AGE)is a key factor of metabolic memory in diabetic patients. The series of studies from ours and others indicated that AGE could promote inflammatory response, oxidative stress, apoptosis and micro-calcification formation in atherosclerotic lesions and accelerate the transition from stable plaque to vulnerable plaque, followed by plaque rupture, thrombogenesis and finally the occurrence of acute coronary syndrome. This paper elaborates the formation, source, metabolism, characterization of AGE and the mechanisms of AGE in inflammation response, lipid accumulation, apoptosis and calcification. We hope it can provide some new ideas for the mechanisms of atherosclerosis and therapeutic strategy.