Diabetes is a worldwide epidemic disease and closely related to cardiovascular diseases such as atherosclerosis (As). In a long-term hyperglycemic environment, a series of complex non-enzymatic glycosylation reactions of proteins, fatty acids and other macromolecular substances in diabetic patients result in the formation of advanced glycosylation end products (AGE). Glycosylated albumin (GA) is the most important form of AGE, which promotes the progression of atherosclerosis by binding to glycosylated product receptor (RAGE) to induce oxidative stress, inflammation and endoplasmic reticulum stress. Therefore, in-depth study of the mechanism of GA-induced atherosclerosis is of great significance to reduce the incidence of cardiovascular events in diabetic patients and delay the disease process. At present, the existed researches have partially revealed its specific mechanisms, and this article reviews the roles of GA in the occurrence and development of atherosclerosis.