Key result
The advanced glycation end product (AGE)-RAGE axis contributes to atrial fibrillation and its thromboembolic complications by evoking inflammatory and fibrotic reactions.
Why the study?
The incidence of AF is higher in patients with diabetes, but the pathological role of AGEs and the AGE-RAGE axis in AF and its thromboembolic complications requires synthesis.
This review highlights the pathological role of the AGE-RAGE axis in promoting atrial fibrillation and thromboembolic complications through inflammatory and fibrotic pathways in diabetic and aging populations.
Accumulating evidence has shown that the incidence of atrial fibrillation (AF) is higher in patients with diabetes, especially those with poor glycemic control or long disease duration. Nonenzymatic 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.
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Yamagishi et al. (2019) studied this question. The advanced glycation end product (AGE)-RAGE axis contributes to atrial fibrillation and its thromboembolic complications by evoking inflammatory and fibrotic reactions.
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