Pathological role of advanced glycation end products (AGEs) and their receptor axis in atrial fibrillation.

Accumulating evidence has shown that incidence of atrial fibrillation (AF) is higher in patients with diabetes, especially those with poor glycemic control or long disease duration. Non-enzymatic glycation of amino acids of proteins, lipids, and nucleic acids has progressed under normal aging process and/or diabetic condition, which could lead to the formation and accumulation of advanced glycation end products (AGEs). AGEs not only alter the tertiary structure and physiological function of macromolecules, but also evoke inflammatory and fibrotic reactions through the interaction of cell surface receptor for AGEs (RAGE), thereby being involved in aging-related disorders. In this paper, we briefly review the association of chronic hyperglycemia and type 1 diabetes with the risk of AF and then discuss the pathological role of AGE-RAGE axis in AF and its thromboembolic complications.