Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease

被引：2380
|
作者：
Hotamisligil, Goekhan S. [1 ,2 ]
机构：
[1] Harvard Univ, Sch Publ Hlth, Dept Nutr, Dept Genet & Complex Dis, Boston, MA 02115 USA
[2] Harvard Univ, Sch Publ Hlth, Broad Inst, Harvard & MIT, Boston, MA 02115 USA
来源：
CELL | 2010年 / 140卷 / 06期
关键词：
UNFOLDED-PROTEIN RESPONSE; NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; PANCREATIC BETA-CELLS; LINKED INSULIN-RESISTANCE; DIET-INDUCED OBESITY; ER STRESS; ADIPOSE-TISSUE; TRANSLATION INITIATION; GLUCOSE-HOMEOSTASIS;
D O I：
10.1016/j.cell.2010.02.034
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The endoplasmic reticulum (ER) is the major site in the cell for protein folding and trafficking and is central to many cellular functions. Failure of the ER's adaptive capacity results in activation of the unfolded protein response (UPR), which intersects with many different inflammatory and stress signaling pathways. These pathways are also critical in chronic metabolic diseases such as obesity, insulin resistance, and type 2 diabetes. The ER and related signaling networks are emerging as a potential site for the intersection of inflammation and metabolic disease.
引用
收藏
页码：900 / 917
页数：18
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