Interleukin-18 and diabetic nephropathy: A review

被引：96
作者：
Yaribeygi, Habib [1 ]
Atkin, Stephen L. [2 ]
Sahebkar, Amirhossein [3 ,4 ,5 ]
机构：
[1] Shahid Beheshti Univ Med Sci, Chron Kidney Dis Res Ctr, Tehran, Iran
[2] Weill Cornell Med Qatar, Doha, Qatar
[3] Mashhad Univ Med Sci, Neurogen Inflammat Res Ctr, Mashhad, Iran
[4] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Biotechnol Res Ctr, Mashhad, Iran
[5] Mashhad Univ Med Sci, Neurogen Inflammat Res Ctr, Mashhad, Iran
来源：
JOURNAL OF CELLULAR PHYSIOLOGY | 2019年 / 234卷 / 05期
关键词：
apoptosis; diabetic nephropathy; inflammatory response; interleukin-18; oxidative stress; tumor necrosis factor-alpha; NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; INTERCELLULAR-ADHESION MOLECULE-1; ISOLATED RAT GLOMERULI; TNF-ALPHA PRODUCTION; GROWTH-FACTOR-BETA; IFN-GAMMA; FAS LIGAND; TGF-BETA; SIGNAL-TRANSDUCTION;
D O I：
10.1002/jcp.27427
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The inflammatory response has an important role in the pathophysiology of diabetic nephropathy that is contributed to by inflammatory mediators such as interleukin-1 (IL-1), IL-6, IL-18, tumor necrosis factor-alpha, and macrophage chemotactic protein-1; however, the role of IL-18 seems to be more specific than other cytokines in the inflammatory process. IL-18 is expressed in renal tissue and is upregulated by several stimuli including hyperglycemia. The expression/urinary level of IL-18 is positively correlated with the progression of diabetic nephropathy and the urinary albumin excretion rate. In this review, we have focused on the molecular pathways modulating the relationship between IL-18 and diabetic nephropathy.
引用
收藏
页码：5674 / 5682
页数：9
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