With Advanced Glycation End Products Induce Tubular Epithelial Cells Express Connective Tissue Growth Factor And Fibronectin

BackgroundThe population of diabetic patients is dramatically increasing in the world. The development of the various complications of diabetes contributes to the high morbidity and mortality. The enlargement of the kidney, large proteinuria excretion, hypertension and damage of kidney function is the major characteristics of diabetic nephropathy. It is well known that, the accumulation of extracellular matrix proteins both in the glomerular mesangium and tubulointerstitium is the typical pathological leisions of diabetic nephropathy; and it is believed from recently studied that, the tubulointerstitial injury may be an important predictor of renal dysfunction in diabetes nephropathy. So the research on the mechanisms of the intiation and development of diabetic tubulointerstitial injuries will be benefit for development of an accurate treatment. It is strongly suggested from recent the in vitro and in vivo studies that AGEs and their receptor (the receptor for AGE, RAGE) system take a crucial part in development of diabetic nephropathy. In diabetic patients, glucose can react non-enzymatically with the amino groups of proteins, lipids and nucleic acids. and form irreversible heterogeneous derivatives termed advanced glycation endproducts (AGEs).after undergoing complex reactions. AGEs are known to accumulate in circulating blood and in various tissues at an extremely accelerated rate under the diabetic state. The structural integrity of the vessel wall and underlying basement membranes were directly influenced through excessive crosslinking of matrix molecules. In addition, receptor-dependent mechanisms are likely to work in the AGE-induced tissue dysfunction and the RAGE (the receptor for AGE) is.the bestcharacterized. The glomerulosclerosis, inflammation infiltration and proteinuria may induce by AGE-RAGE interaction. The underlying pathogenic link between AGEs and the development of tubulointerstitial injury has not widely been investigated yet and the nechanism of AGEs mediated tubulointerstitial injury still waiting for elucidation.