作者: Kailash Prasad , None
关键词:
摘要: Atrial fibrillation (AF) is the most common of cardiac arrhythmias. Mechanisms such as atrial structural remodeling and electrical have been implicated in pathogenesis AF. The data to date suggest that advanced glycation end products (AGEs) its cell receptor RAGE (receptor for AGE) soluble (sRAGE) are involved This review focuses on role AGE–RAGE axis Interaction AGE with generates reactive oxygen species, cytokines, vascular adhesion molecules. sRAGE a cytoprotective agent. show serum levels sRAGE, expression RAGE, elevated AF patients. Elevated did not protect development might be due greater elevation than sRAGE. Measurement stress (AGE/sRAGE) would appropriate compared measurement or alone interaction can induce through alteration cellular protein extracellular matrix. remodeling. treatment strategy should directed toward reduction levels, suppression expression, blocking binding antioxidants. In conclusion, modalities include lowering AGE, use