title: Advanced glycation end product (age) inhibitors and their therapeutic implications in diseases.
abstract: Nonenzymatic modification of proteins by reducing sugars, a process that is also known as the Maillard reaction, leads to the formation of advanced glycation end products (AGEs) in vivo. There is a growing body of evidence that formation and accumulation of AGEs progress during normal aging, and at an extremely accelerated rate under diabetes, and are thus involved in the pathogenesis of various diseases such as diabetic vascular complications and neurodegenerative diseases. Therefore, inhibition of AGE formation may be a promising target for therapeutic intervention in AGE-related disorders. In this review, we discuss several types of AGE inhibitors and their therapeutic implications in diseases.
authors.affiliation: Department of Biochemistry, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Takeuchi
authors.forename: S
authors.initials: S
authors.lastname: Yamagishi
authors.forename: M
authors.initials: M
authors.lastname: Iwaki
authors.forename: K
authors.initials: K
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Imaizumi
mesh_terms: D000818:Animals; D002626:Chemistry, Pharmaceutical; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors* / Q000627:therapeutic use*; D006801:Humans; D019636:Neurodegenerative Diseases / Q000188:drug therapy; D016032:Randomized Controlled Trials as Topic
chemical_list: D017127:Glycation End Products, Advanced