Implications of Treatment That Target Protective Mechanisms Against Diabetic Nephropathy

被引:38
作者
Mima, Akira [1 ]
Qi, Weier [1 ]
King, George L. [1 ]
机构
[1] Harvard Univ, Sch Med, Dianne Normally Hoppes Lab Diabet Complicat, Res Div,Joslin Diabet Ctr, Boston, MA 02215 USA
基金
美国国家卫生研究院;
关键词
Hyperglycemia; protein kinase C (PKC)beta; advanced glycation end products (AGEs); platelet-derived growth factor (PDGF); vascular endothelial growth factor (VEGF); ENDOTHELIAL GROWTH-FACTOR; KINASE-C-BETA; ALDOSE REDUCTASE INHIBITOR; NITRIC-OXIDE SYNTHASE; INSULIN-RESISTANCE; RENAL INJURY; REDUCES PROTEINURIA; OXIDATIVE STRESS; RANDOMIZED-TRIAL; ACTIVATION;
D O I
10.1016/j.semnephrol.2012.07.010
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Diabetes results in vascular changes and dysfunction, and vascular complications are the leading cause of morbidity and mortality in diabetic patients. There has been a continual increase in the number of diabetic nephropathy patients and epidemic increases in the number of patients progressing to end-stage renal diseases. To identify targets for therapeutic intervention, most studies have focused on understanding how abnormal levels of glucose metabolites cause diabetic nephropathy, which is of paramount importance in devising strategies to combat the development and progression of diabetic nephropathy. However, less studied than the systemic toxic mechanisms, hyperglycemia and dyslipidemia might inhibit the endogenous vascular protective factors such as insulin, vascular endothelial growth factor, and platelet-derived growth factor. In this review, we highlight the importance of enhancing endogenous protective factors to prevent or delay diabetic nephropathy.© 2012 Elsevier Inc.
引用
收藏
页码:471 / 478
页数:8
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