Recent advances in understanding the biochemical and molecular mechanism of diabetic nephropathy

被引:272
作者
Sun, Yan-Ming [1 ]
Su, Ying [2 ]
Li, Jia [1 ]
Wang, Lan-Feng [1 ]
机构
[1] Harbin Med Univ, Dept Cardiac Care Unit, Affiliated Hosp 1, Harbin 150001, Peoples R China
[2] Harbin Med Univ, Dept Endocrinol, Affiliated Hosp 1, Harbin 150001, Peoples R China
基金
中国国家自然科学基金;
关键词
Diabetic nephropathy; Hyperglycemia; Advanced glycation end products; Protein kinase C; Oxidative stress; ACTIVATED RECEPTOR-GAMMA; GLYCATION END-PRODUCTS; OXIDATIVE STRESS; PPAR-GAMMA; PROGRESSION; COLLAGEN; COMPLICATIONS; SPECTROSCOPY; INFLAMMATION; MACROPHAGES;
D O I
10.1016/j.bbrc.2013.02.120
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Diabetic nephropathy (DN) is a chronic disease characterized by proteinuria, glomerular hypertrophy, decreased glomerular filtration and renal fibrosis with loss of renal function. DN is the leading cause of end-stage renal disease, accounting for millions of deaths worldwide. Hyperglycemia is the driving force for the development of diabetic nephropathy. The exact cause of diabetic nephropathy is unknown, but various postulated mechanisms are: hyperglycemia (causing hyperfiltration and renal injury), advanced glycosylation products, activation of cytokines. In this review article, we have discussed a number of diabetes-induced metabolites such as glucose, advanced glycation end products, protein kinase C and oxidative stress and other related factors that are implicated in the pathophysiology of the DN. An understanding of the biochemical and molecular changes especially early in the DN may lead to new and effective therapies towards prevention and amelioration of DN. (C) 2013 Published by Elsevier Inc.
引用
收藏
页码:359 / 361
页数:3
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