炎症在糖尿病肾病发病机制中的作用

被引：41

作者：

陈霞

王锋

汪年松

机构：

[1] 上海交通大学附属第六人民医院肾脏内科

来源：

中国中西医结合肾病杂志 | 2017年 / 18卷 / 07期

关键词：

D O I：

暂无

中图分类号：

R587.2 [糖尿病性昏迷及其他并发症]; R692.9 [其他疾病];

学科分类号：

100201 [内科学]; 100221 [泌尿外科学];

摘要：

<正>近年来,随着糖尿病发病率的逐年升高,糖尿病的常见并发症——糖尿病肾病（diabetic nephropathy,DN）所导致的终末期肾衰竭威胁着越来越多的人群[1～3]。DN具体发病机制尚不明确,目前普遍认为DN发病是生化代谢紊乱、肾小球血液动力学改变、氧化应激、细胞因子与遗传易感性等多因素共同作用的结果,然而以上发病机制仍不足以解释糖尿病肾脏的病理改变[2,5]。近年来,在探索病因时,不少学者提出了炎症机制学

引用

页码：637 / 640

页数：4

共 16 条

[1]

Broad Infiltration of Macrophages Leads to a Proinflammatory State in Streptozotocin-Induced Hyperglycemic Mice [J].

Niu, Shuo ;

Bian, Zhen ;

Tremblay, Alexandra ;

Luo, Youqun ;

Kidder, Koby ;

Mansour, Ahmed ;

Zen, Ke ;

Liu, Yuan .

JOURNAL OF IMMUNOLOGY, 2016, 197 (08) :3293-3301

[2]

High glucose induces rat mesangial cells proliferation and MCP-1 expression via ROS-mediated activation of NF-κB pathway, which is inhibited by eleutheroside E [J].

Yang, Xiuqin ;

Wang, Yangang ;

Gao, Guanqi .

JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION, 2016, 36 (02) :152-157

[3]

Effects of ROS-relative NF-κB signaling on high glucose-induced TLR4 and MCP-1 expression in podocyte injury [J].

Wei Miaomiao ;

Li Zhigui ;

Xiao Lu ;

Yang Zhuo .

MOLECULAR IMMUNOLOGY, 2015, 68 (02) :261-271

[4]

Differential impact of glucose levels and advanced glycation end-products on tubular cell viability and pro-inflammatory/profibrotic functions [J].

Franko, Benoit ;

Brault, Julie ;

Jouve, Thomas ;

Beaumel, Sylvain ;

Benhamou, Pierre-Yves ;

Zaoui, Philippe ;

Stasia, Marie Jose .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2014, 451 (04) :627-631

[5]

Microinflammation in the pathogenesis of diabetic nephropathy [J].

Shikata, Kenichi ;

Makino, Hirofumi .

JOURNAL OF DIABETES INVESTIGATION, 2013, 4 (02) :142-149

[6]

d -Saccharic acid 1;4-lactone protects diabetic rat kidney by ameliorating hyperglycemia-mediated oxidative stress and renal inflammatory cytokines via NF-κB and PKC signaling.[J].Semantee Bhattacharya;Prasenjit Manna;Ratan Gachhui;Parames C. Sil.Toxicology and Applied Pharmacology.2012,

[7]

Attenuation of diabetic nephropathy in diabetes rats induced by streptozotocin by regulating the endoplasmic reticulum stress inflammatory response [J].

Qi, Wei ;

Mu, Jiao ;

Luo, Zhi-Feng ;

Zeng, Wei ;

Guo, Yan-Hong ;

Pang, Qi ;

Ye, Zi-Lin ;

Liu, Li ;

Yuan, Fa-Huan ;

Feng, Bing .

METABOLISM-CLINICAL AND EXPERIMENTAL, 2011, 60 (05) :594-603

[8]

Effects of 4-phenylbutyric acid on the process and development of diabetic nephropathy induced in rats by streptozotocin: Regulation of endoplasmic reticulum stress-oxidative activation.[J].Zhi-Feng Luo;Bing Feng;Jiao Mu;Wei Qi;Wei Zeng;Yan-Hong Guo;Qi Pang;Zi-Lin Ye;Li Liu;Fa-Huan Yuan.Toxicology and Applied Pharmacology.2010, 1

[9]

Activation of Protein Kinase C Isoforms and Its Impact on Diabetic Complications [J].

Geraldes, Pedro ;

King, George L. .

CIRCULATION RESEARCH, 2010, 106 (08) :1319-1331

[10]

Tumor necrosis factor-α as a therapeutic target for diabetic nephropathy [J].

Navarro-Gonzalez, Juan F. ;

Jarque, Ana ;

Muros, Mercedes ;

Mora, Carmen ;

Garcia, Javier .

CYTOKINE & GROWTH FACTOR REVIEWS, 2009, 20 (02) :165-173

← 1 2 →