SIRT1: Mechanism and Protective Effect in Diabetic Nephropathy

被引:32
作者
Ji, Jing [1 ]
Tao, Pengyu [2 ]
Wang, Qian [3 ]
Li, Lingxing [4 ]
Xu, Yuzhen [5 ]
机构
[1] Shanghai Univ Tradit Chinese Med, Yueyang Hosp, Dept Nephrol, Shanghai 200437, Peoples R China
[2] Shanghai Univ Tradit Chinese Med, Basic Med Sch, Shanghai 200120, Peoples R China
[3] Shandong First Med Univ & Shandong Acad Med Sci, Taian City Cent Hosp, Dept Cent Lab, Tai An, Shandong, Peoples R China
[4] Shandong First Med Univ & Shandong Acad Med Sci, Taian City Cent Hosp, Dept Cardiovasc Med, Tai An 271000, Shandong, Peoples R China
[5] Tongji Univ, Sch Med, Shanghai Peoples Hosp 10, Dept Neurol, 301 Middle Yanchang Rd, Shanghai 200072, Peoples R China
基金
美国国家科学基金会;
关键词
Diabetic nephropathy; SIRT1; inflammation; calorie restriction; acetylation; ESRD; CELLULAR SENESCENCE; THERAPEUTIC TARGET; INDUCED APOPTOSIS; OXIDATIVE STRESS; STEM-CELLS; RESVERATROL; PATHWAY; HYPOXIA; ACTIVATION; AUTOPHAGY;
D O I
10.2174/1871530320666201029143606
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Diabetic nephropathy (DN) is referred to as the microvascular complication of the kidneys induced by insufficient production of insulin or an ineffective cellular response to insulin, and is the main cause of end-stage renal disease. Currently, available therapies provide only symptomatic relief and fail to improve the outcome of diabetic nephropathy. Studies on diabetic animals had shown overexpression of SIRT1 in both podocytes and renal tubular cells attenuated proteinuria and kidney injury in the animal model of DN. Sirt1 exerts renoprotective effects in DKD in part through the deacetylation of transcription factors involved in the disease pathogenesis, such as NF-kappa B, Smad3, FOXO and p53. The purpose of this review is to highlight the protective mechanism of SIRT1 involved in the pathogenesis of diabetic nephropathy.
引用
收藏
页码:835 / 842
页数:8
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