scholarly journals Advanced Glycation end Products, Oxidative Stress and Diabetic Nephropathy

2010 ◽  
Vol 3 (2) ◽  
pp. 101-108 ◽  
Author(s):  
Sho-ichi Yamagishi ◽  
Takanori Matsui
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Stress Generation ◽  
Stress System ◽  
Diabetic Patients ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Stage Renal Disease

About 246 million people worldwide had diabetes in 2007. The global figure of people with diabetes is projected to increase to 370 million in 2030. As the prevalence of diabetes has risen to epidemic proportions worldwide, diabetic nephropathy has become one of the most challenging health problems. Therapeutic options such as strict blood glucose and blood pressure controls are effective for preventing diabetic nephropathy, but are far from satisfactory, and the number of diabetic patients on end-stage renal disease is still increasing. Therefore, a novel therapeutic strategy that could halt the progression of diabetic nephropathy should be developed. There is accumulating evidence that advanced glycation end products (AGEs), senescent macroprotein derivatives formed at an accelerated rate under diabetes, play a role in diabetic nephropathy via oxidative stress generation. In this paper, we review the pathophysiological role of AGEs and their receptor (RAGE)-oxidative stress system in diabetic nephropathy.

Flavonoids derived from buckwheat hull break advanced glycation end-products and improve diabetic nephropathy

2021 ◽  
Author(s):  
Tianzhu Li ◽  
Yuying Yang ◽  
Xiujuan Wang ◽  
Weichang Dai ◽  
Lan Zhang ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Diabetic Patients ◽  
Advanced Glycation ◽  
Important Complication ◽  
Glycation End Products ◽  
End Products

Diabetic nephropathy (DN) is the most important complication of diabetic patients. The accumulation of advanced glycation end-products (AGEs) is the main reason for the development of DN. This study investigated...

scholarly journals 3′-O-β-d-glucopyranosyl-α,4,2′,4′,6′-pentahydroxy-dihydrochalcone, from Bark of Eysenhardtia polystachya Prevents Diabetic Nephropathy via Inhibiting Protein Glycation in STZ-Nicotinamide Induced Diabetic Mice

Molecules ◽  
2019 ◽  
Vol 24 (7) ◽  
pp. 1214 ◽  
Author(s):  
Rosa Pérez Gutierrez ◽  
Abraham García Campoy ◽  
Silvia Paredes Carrera ◽  
Alethia Muñiz Ramirez ◽  
José Mota Flores ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Renal Damage ◽  
Histological Analysis ◽  
Protein Glycation ◽  
Diabetic Patients ◽  
Diabetic Mice ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Previous studies have shown that accumulation of advanced glycation end products (AGEs) can be the cause of diabetic nephropathy (DN) in diabetic patients. Dihydrochalcone 3′-O-β-d-glucopyranosyl α,4,2′,4′,6′-pentahydroxy–dihydrochalcone (1) is a powerful antiglycation compound previously isolated from Eysenhardtia polystachya. The aim was to investigate whether (1) was able to protect against diabetic nephropathy in streptozotocin (STZ)-induced diabetic mice, which displayed renal dysfunction markers such as body weight, creatinine, uric acid, serum urea, total urinary protein, and urea nitrogen in the blood (BUN). In addition, pathological changes were evaluated including glycated hemoglobin (HbA1c), advanced glycation end products (AGEs) in the kidney, as well as in circulation level and pro-inflammatory markers ICAM-1 levels in diabetic mice. After 5 weeks, these elevated markers of dihydrochalcone treatment (25, 50 and 100 mg/kg) were significantly (p < 0.05) attenuated. In addition, they ameliorate the indices of renal inflammation as indicated by ICAM-1 markers. The kidney and circulatory AGEs levels in diabetic mice were significantly (p < 0.05) attenuated by (1) treatment. Histological analysis of kidney tissues showed an important recovery in its structure compared with the diabetic group. It was found that the compound (1) attenuated the renal damage in diabetic mice by inhibiting AGEs formation.

Advanced glycation end products mediated cellular and molecular events in the pathology of diabetic nephropathy

2016 ◽  
Vol 7 (5-6) ◽  
pp. 293-309 ◽  
Author(s):  
Anil Kumar Pasupulati ◽  
P. Swathi Chitra ◽  
G. Bhanuprakash Reddy
Keyword(s):  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Basement Membranes ◽  
Renal Outcome ◽  
Diabetic Patients ◽  
Advanced Glycation ◽  
Mesenchymal Transition ◽  
Molecular Events ◽  
Glycation End Products ◽  
End Products

AbstractDiabetic nephropathy (DN) is a major cause of morbidity and mortality in diabetic patients and a leading cause of end-stage renal disease (ESRD). Degenerative changes such as glomerular hypertrophy, hyperfiltration, widening of basement membranes, tubulointerstitial fibrosis, glomerulosclerosis and podocytopathy manifest in various degrees of proteinuria in DN. One of the key mechanisms implicated in the pathogenesis of DN is non-enzymatic glycation (NEG). NEG is the irreversible attachment of reducing sugars onto free amino groups of proteins by a series of events, which include the formation of Schiff’s base and an Amadori product to yield advanced glycation end products (AGEs). AGE modification of client proteins from the extracellular matrix induces crosslinking, which is often associated with thickening of the basement membrane. AGEs activate several intracellular signaling cascades upon interaction with receptor for AGEs (RAGE), which manifest in aberrant cellular responses such as inflammation, apoptosis and autophagy, whereas other receptors such as AGE-R1, AGE-R3 and scavenger receptors also bind to AGEs and ensue endocytosis and degradation of AGEs. Elevated levels of both serum and tissue AGEs are associated with adverse renal outcome. Increased evidence supports that attenuation of AGE formation and/or inhibition of RAGE activation manifest(s) in improving renal function. This review provides insights of NEG, discusses the cellular and molecular events triggered by AGEs, which manifest in the pathogenesis of DN including renal fibrosis, podocyte epithelial-mesenchymal transition and activation of renin-angiotensin system. Therapies designed to target AGEs, such as inhibitors of AGEs formation and crosslink breakers, are discussed.

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