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Metabolism of inflammation limited by AMPK and pseudo-starvation

机译:AMPK和假饥饿限制了炎症的代谢

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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 la 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.
机译:参与炎症的细胞(例如活化的巨噬细胞和T-helper 17细胞)的代谢变化包括葡萄糖吸收增加,糖酵解和戊糖磷酸途径活性增加。已经提出了在针对缺氧诱导因子Ia和AMP激活的蛋白激酶的这些变化中相反的作用。相反,抗炎细胞,例如M2巨噬细胞,调节性T细胞和静态记忆T细胞,具有较低的糖酵解速率和较高的氧化代谢水平。某些抗炎药可能通过激活AMP激活的蛋白激酶来诱导类似于假饥饿的状态。因此,新陈代谢的改变可能参与了促进或抑制炎症的信号导向程序。

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  • 来源
    《Nature》 |2013年第7432期|346-355|共10页
  • 作者单位

    School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Ireland;

    Division of Cell Signalling and Immunology, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
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