THE ROLE OF ADVANCED GLYCATION END PRODUCTS IN PATOGENESIS OF DIABETIC NEPHROPATHY

被引：2
作者：
Gavrilova, Alina O. [1 ]
Severina, Anastasia S. [1 ]
Shamhalova, Minara S. [1 ]
Shestakova, Marina, V [1 ]
机构：
[1] Endocrinol Res Ctr, Moscow, Russia
来源：
DIABETES MELLITUS | 2021年 / 24卷 / 05期
关键词：
advanced glycation end products; metabolic memory; diabetic nephropathy; diabetes mellitus; CIRCULATING SOLUBLE RECEPTOR; OXIDATIVE STRESS; GENE-EXPRESSION; MESANGIAL MATRIX; PLASMA-LEVELS; RAGE; AGES; ACCUMULATION; PREVENTION; PODOCYTES;
D O I：
10.14341/DM12784
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Diabetes mellitus (DM) and chronic kidney disease are the diseases that have exceeded epidemic thresholds in terms of prevalence all over the world. That made it possible to classify them as non-communicable epidemics of the XXI century. Diabetic nephropathy (DN) is implicated with high levels of disablement and mortality. Advanced glycation end products (AGE) play a key role in the progression of DN. Increased formation of AGE occurs due to hyperglycemia under the conditions of diabetes. Moreover, there are additional factors in DN that increase the elaboration of AGE, such as high levels of oxidative stress and decreased renal clearance which slows down the AGE excretion. Both immediate effects of AGE and interaction of AGE with its cell-bound receptor (RAGE) result in a cascade of events that lead to further progression of DN. Thus, the research of the new therapeutic approaches targeted on the AGE-RAGE system is of great interest to slow progression of DN and improve the prognosis.
引用
收藏
页码：461 / 469
页数：9
相关论文
共 79 条
[51]   Crosstalk between Advanced Glycation and Endoplasmic Reticulum Stress: Emerging Therapeutic Targeting for Metabolic Diseases [J].
Piperi, Christina ;
Adamopoulos, Christos ;
Dalagiorgou, Georgia ;
Diamanti-Kandarakis, Evanthia ;
Papavassiliou, Athanasios G. .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2012, 97 (07) :2231-2242
[52]   Is there any evidence that AGE/sRAGE is a universal biomarker/risk marker for diseases? [J].
Prasad, Kailash .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 2019, 451 (1-2) :139-144
[53]  
Prasad K, 2017, INT J ANGIOL, V26, P1, DOI 10.1055/s-0037-1598183
[54]   Evidence that pioglitazone, metformin and pentoxifylline are inhibitors of glycation [J].
Rahbar, S ;
Natarajan, R ;
Yerneni, KK ;
Scott, S ;
Gonzales, N ;
Nadler, JL .
CLINICA CHIMICA ACTA, 2000, 301 (1-2) :65-77
[55]   Receptor for AGE (RAGE): signaling mechanisms in the pathogenesis of diabetes and its complications [J].
Ramasamy, Ravichandran ;
Yan, Shi Fang ;
Schmidt, Ann Marie .
YEAR IN DIABETES AND OBESITY, 2011, 1243 :88-102
[56]   Recombinant advanced glycation end product receptor pharmacokinetics in normal and diabetic rats [J].
Renard, C ;
Chappey, O ;
Wautier, MP ;
Nagashima, M ;
Lundh, E ;
Morser, J ;
Zhao, L ;
Schmidt, AM ;
Scherrmann, JM ;
Wautier, JL .
MOLECULAR PHARMACOLOGY, 1997, 52 (01) :54-62
[57]  
Schiffer M, 2001, J CLIN INVEST, V108, P807, DOI 10.1172/JCI12367
[58]   The podocyte's response to injury: Role in proteinuria and glomerulosclerosis [J].
Shankland, S. J. .
KIDNEY INTERNATIONAL, 2006, 69 (12) :2131-2147
[59]   NONENZYMATIC GLYCATION OF MESANGIAL MATRIX AND PROLONGED EXPOSURE OF MESANGIAL MATRIX TO ELEVATED GLUCOSE REDUCES COLLAGEN-SYNTHESIS AND PROTEOGLYCAN CHARGE [J].
SILBIGER, S ;
CROWLEY, S ;
SHAN, Z ;
BROWNLEE, M ;
SATRIANO, J ;
SCHLONDORFF, D .
KIDNEY INTERNATIONAL, 1993, 43 (04) :853-864
[60]  
Striker LJ, 1996, NEPHROL DIAL TRANSPL, V11, P62
12345678