β-Cell inflammation in human type 2 diabetes and the role of autophagy

被引：35
作者：
Marselli, L. [1 ]
Bugliani, M. [1 ]
Suleiman, M. [1 ]
Olimpico, F. [1 ]
Masini, M. [2 ]
Petrini, M. [1 ]
Boggi, U. [2 ]
Filipponi, F. [3 ]
Syed, F. [1 ]
Marchetti, P. [1 ]
机构：
[1] Univ Pisa, Dept Clin & Expt Med, I-56124 Pisa, Italy
[2] Univ Pisa, Dept Translat Res & New Technol Med & Surg, I-56124 Pisa, Italy
[3] Univ Pisa, Dept Surg Pathol Med Mol & Crit Area, I-56124 Pisa, Italy
来源：
DIABETES OBESITY & METABOLISM | 2013年 / 15卷
关键词：
autophagy; inflammation; pancreatic islets; type; 2; diabetes; beta-cells; ISLET-ASSOCIATED MACROPHAGES; GENE-EXPRESSION; IL-1-BETA; GLUCOSE; GLUCOTOXICITY; INTERLEUKIN-1; MECHANISMS; APOPTOSIS; HEALTH; FAMILY;
D O I：
10.1111/dom.12152
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
beta-Cell failure is crucial for the onset and progression of human type 2 diabetes, and a few studies have suggested that inflammation may play a role. Immune cell infiltration has been reported in subpopulations of islets in some cases of human type 2 diabetes, and altered gene expression of a few cytokines and chemokines has been observed in isolated islets and laser captured beta-cells from diabetic subjects. Recent observations on the links between inflammation, apoptosis and autophagy are putting the focus on the possibility that modulating the autophagic processes could protect the beta-cells from cytotoxicity induced by inflammatory mediators.
引用
收藏
页码：130 / 136
页数：7
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