Molecular mechanisms in the pathogenesis of diabetic nephropathy: An update

被引:199
作者
Arora, Mandeep Kumar [1 ]
Singh, Umesh Kumar [1 ]
机构
[1] Swami Vivekanand Subharti Univ, Fac Pharm, Meerut 250005, Uttar Pradesh, India
关键词
Diabetic nephropathy; Renal fibrosis; Target site; Signaling pathways; GROWTH-FACTOR-BETA; PROTEIN-KINASE-C; TUMOR-NECROSIS-FACTOR; PLASMINOGEN-ACTIVATOR INHIBITOR-1; GLOMERULAR MESANGIAL CELLS; VASCULAR SMOOTH-MUSCLE; NITRIC-OXIDE SYNTHASE; MONOCYTE CHEMOATTRACTANT PROTEIN-1; ANGIOTENSIN-ALDOSTERONE SYSTEM; JAK/STAT SIGNALING PATHWAY;
D O I
10.1016/j.vph.2013.01.001
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Diabetes mellitus is known to trigger retinopathy, neuropathy and nephropathy. Diabetic nephropathy, a long-term major microvascular complication of uncontrolled hyperglycemia, affects a large population worldwide. Recent findings suggest that numerous pathways are activated during the course of diabetes mellitus and that these pathways individually or collectively play a role in the induction and progression of diabetic nephropathy. However, clinical strategies targeting these pathways to manage diabetic nephropathy remain unsatisfactory, as the number of diabetic patients with nephropathy is increasing yearly. To develop ground-breaking therapeutic options to prevent the development and progression of diabetic nephropathy, a comprehensive understanding of the molecular mechanisms involved in the pathogenesis of the disease is mandatory. Therefore, the purpose of this paper is to discuss the underlying mechanisms and downstream pathways involved in the pathogenesis of diabetic nephropathy. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:259 / 271
页数:13
相关论文
共 196 条
[1]   Signalling pathways of the TNF superfamily: A double-edged sword [J].
Aggarwal, BB .
NATURE REVIEWS IMMUNOLOGY, 2003, 3 (09) :745-756
[2]   ACE inhibitors improve diabetic nephropathy through suppression of renal MCP-1 [J].
Amann, B ;
Tinzmann, R ;
Angelkort, B .
DIABETES CARE, 2003, 26 (08) :2421-2425
[3]   Angiotensin II activation of the JAK/STAT pathway in mesangial cells is altered by high glucose [J].
Amiri, F ;
Shaw, S ;
Wang, XD ;
Tang, J ;
Waller, JL ;
Eaton, DC ;
Marrero, MB .
KIDNEY INTERNATIONAL, 2002, 61 (05) :1605-1616
[4]  
[Anonymous], METABOLISM
[5]   The low dose combination of fenofibrate and rosiglitazone halts the progression of diabetes-induced experimental nephropathy [J].
Arora, Mandeep Kumar ;
Reddy, Krishna ;
Balakumar, Pitchai .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2010, 636 (1-3) :137-144
[6]   Effects of NADPH oxidase inhibitor in diabetic nephropathy [J].
Asaba, K ;
Tojo, A ;
Onozato, ML ;
Goto, A ;
Quinn, MT ;
Fujita, T ;
Wilcox, CS .
KIDNEY INTERNATIONAL, 2005, 67 (05) :1890-1898
[7]   Evidence for a role of Rho-like GTPases and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) in transforming growth factor beta-mediated signaling [J].
Atfi, A ;
Djelloul, S ;
Chastre, E ;
Davis, RR ;
Gespach, C .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (03) :1429-1432
[8]   Adenosine A2A receptor activation attenuates inflammation and injury in diabetic nephropathy [J].
Awad, AS ;
Huang, LP ;
Ye, H ;
Duong, ETA ;
Bolton, WK ;
Linden, J ;
Okusa, MD .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2006, 290 (04) :F828-F837
[9]   Altered expression and subcellular localization of diacylglycerol-sensitive protein kinase C isoforms in diabetic rat glomerular cells [J].
Babazono, T ;
Kapor-Drezgic, J ;
Dlugosz, JA ;
Whiteside, C .
DIABETES, 1998, 47 (04) :668-676
[10]   NADPH oxidase [J].
Babior, BM .
CURRENT OPINION IN IMMUNOLOGY, 2004, 16 (01) :42-47