Microvascular Complications Associated with Advanced Glycation End Products in Diabetes

Abstract

Diabetes is a frequent metabolic complaint associated with increasing blood sugar levels, it also has a connection to long- term vascular problems that can damage blood vessels, urinary tract, sight, and neurons. By adding amino acid breakdown and ultimately accumulating complex end products of glycation in the organs, hyperglycemia is a crucial factor in the progression of complications related to diabetes. The breakdown process, which entails free of enzymes couplings of polysaccharides to lipids, proteins, or inheritable material, produces miscellaneous motes known to be sophisticated glycation end products. The root cause of diabetes-related difficulties such as atherosclerosis, retinopathy, nephropathy, and nephropathy are greatly impacted by the development of complex end products of glycation and the glycation of proteins. Glycation of proteins hinders molecules from behaving as anticipated by altering the functioning of enzymes, altering the structure of molecules, and impeding sensory interaction. In order to aid in the development of diabetes problems. Recent research suggests that AGEs interact with RAGEs on the plasma membrane to change gene expression, intracellular signaling, and the release of free radicals and pro-inflammatory chemicals. The formation of several AGE types from the glycation of plasma proteins is covered in the current review. The pathogenesis of diabetes sequelae such as retinal degeneration, glaucoma nerve damage, kidney failure, and myocardium are also discussed in relation to AGEs. This study includes an update on the disease's vascular consequences, underlying causes, and available therapeutic options. A summary of illness management techniques is also provided in this article.