Expression of advanced glycation end products and their cellular receptor RAGE in diabetic nephropathy and nondiabetic renal disease
N Tanji, GS Markowitz, C Fu, T Kislinger… - Journal of the …, 2000 - journals.lww.com
Advanced glycation end products (AGE) contribute to diabetic tissue injury by two major
mechanisms, ie, the alteration of extracellular matrix architecture through nonenzymatic
glycation, with formation of protein crosslinks, and the modulation of cellular functions
through interactions with specific cell surface receptors, the best characterized of which is
the receptor for AGE (RAGE). Recent evidence suggests that the AGE-RAGE interaction may
also be promoted by inflammatory processes and oxidative cellular injury. To characterize …
mechanisms, ie, the alteration of extracellular matrix architecture through nonenzymatic
glycation, with formation of protein crosslinks, and the modulation of cellular functions
through interactions with specific cell surface receptors, the best characterized of which is
the receptor for AGE (RAGE). Recent evidence suggests that the AGE-RAGE interaction may
also be promoted by inflammatory processes and oxidative cellular injury. To characterize …