Receptor for advanced glycation end products (AGEs) (RAGE) plays a central role in the process of plaque rupture in diabetic patients. Recently, it has been reported that RAGE may be downregulated by improving glycemic control. In contrast, despite being well known that RAGE may be induced in human vessels in a glucose-independent fashion, also by myeloperoxidase (MPO)-dependent AGE generation, no data exist regarding the possibility of a pharmacological modulation of glucose-independent RAGE generation. Thus, the aim of this study was to characterize the effect of simvastatin on the expression of RAGE and RAGE-dependent plaque-destabilizing genes in human atherosclerotic plaques.
Cuccurullo, C., Iezzi, A., Fazia, M., De Cesare, D., Di Francesco, A., Muraro, R., et al. (2006). Suppression of RAGE as a basis of simvastatin-dependent plaque stabilization in type 2 diabetes. ARTERIOSCLEROSIS, THROMBOSIS, AND VASCULAR BIOLOGY, 26(12), 2716-2723 [10.1161/01.ATV.0000249630.02085.12].
Suppression of RAGE as a basis of simvastatin-dependent plaque stabilization in type 2 diabetes
BEI, ROBERTO;
2006-12-01
Abstract
Receptor for advanced glycation end products (AGEs) (RAGE) plays a central role in the process of plaque rupture in diabetic patients. Recently, it has been reported that RAGE may be downregulated by improving glycemic control. In contrast, despite being well known that RAGE may be induced in human vessels in a glucose-independent fashion, also by myeloperoxidase (MPO)-dependent AGE generation, no data exist regarding the possibility of a pharmacological modulation of glucose-independent RAGE generation. Thus, the aim of this study was to characterize the effect of simvastatin on the expression of RAGE and RAGE-dependent plaque-destabilizing genes in human atherosclerotic plaques.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
