Metabolism of inflammation limited by AMPK and pseudo-starvation

被引:1049
作者
O'Neill, Luke A. J. [1 ]
Hardie, D. Grahame [2 ]
机构
[1] Trinity Coll Dublin, Trinity Biomed Sci Inst, Sch Biochem & Immunol, Dublin, Ireland
[2] Univ Dundee, Coll Life Sci, Div Cell Signalling & Immunol, Dundee DD1 5EH, Scotland
基金
爱尔兰科学基金会; 英国惠康基金; 欧洲研究理事会;
关键词
ACTIVATED PROTEIN-KINASE; FATTY-ACID OXIDATION; T-CELL MEMORY; 5-AMINOIMIDAZOLE-4-CARBOXAMIDE RIBONUCLEOSIDE; MACROPHAGE POLARIZATION; COACTIVATOR PGC-1-BETA; MAMMALIAN TARGET; YEAST SNF1; GLUCOSE; PHOSPHORYLATION;
D O I
10.1038/nature11862
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
Metabolic changes in cells that participate in inflammation, such as activated macrophages and T-helper 17 cells, include a shift towards enhanced glucose uptake, glycolysis and increased activity of the pentose phosphate pathway. Opposing roles in these changes for hypoxia-inducible factor 1 alpha and AMP-activated protein kinase have been proposed. By contrast, anti-inflammatory cells, such as M2 macrophages, regulatory T cells and quiescent memory T cells, have lower glycolytic rates and higher levels of oxidative metabolism. Some anti-inflammatory agents might act by inducing, through activation of AMP-activated protein kinase, a state akin to pseudo-starvation. Altered metabolism may thus participate in the signal-directed programs that promote or inhibit inflammation.
引用
收藏
页码:346 / 355
页数:10
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