[Therapeutic intervention in diseases with advanced glycation end products in their pathogenesis]

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 (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, neurodegenerative diseases, renal failure, and liver cirrhosis. Therefore, inhibition of AGEs formation may be a promising target for therapeutic intervention in AGEs-related disorders. There is a growing body of evidence that AGEs and their receptor (receptor for advanced glycation endproducts--RAGE) axis are also implicated in the pathogenesis of various diseases. In the former part of this paper, we discuss several types of AGEs inhibitors and their therapeutic implications in diseases. Then we summarize in the latter part of this review recent findings regarding pathophysiological roles in diseases of RAGE and soluble RAGE and discuss their potential usefulness as therapeutic targets.