The influence of toxic advanced glycation end-products (TAGEs) on the development of diabetic nephropathy

Abstract

Acquired blindness, end-stage renal failure, accelerated atherosclerosis, and other neuropathies are all primarily caused by diabetic complications. Through a variety of metabolic disturbances, chronic hyperglycaemia plays a primary role in the ethiology of diabetic micro- and macrovascular problems. The synthesis of several kinds of advanced glycation end products (AGEs) was enhanced by high glucose. It was recently shown that AGEs (AGE-2) produced from glyceraldehyde are crucial to the pathophysiology of angiopathy in diabetic individuals. The receptor for AGEs (RAGE), which is present on a variety of cell types in diabetes-affected cells, is of great interest. According to recent research, the interaction between RAGE and AGE-2, which is primarily the structure of toxic AGEs or TAGE, can change gene expression, intracellular signalling, the release of pro-inflammatory molecules, and the generation of reactive oxygen species (ROS), all of which are factors in the pathophysiology of diabetic complications. The pathophysiology of diabetic complications involves factors such as gene expression, intracellular signalling, the release of pro-inflammatory molecules, and the generation of reactive oxygen species (ROS). Recent research indicates that the interaction between RAGE and AGE-2, which is primarily the structure of toxic AGEs or TAGE, can affect these processes.