School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Ireland.
Nature. 2013 Jan 17;493(7432):346-55. doi: 10.1038/nature11862.
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 1α 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.
参与炎症反应的细胞（如激活的巨噬细胞和 Th17 细胞）的代谢变化包括向增强的葡萄糖摄取、糖酵解和增加的戊糖磷酸途径活性转变。已经提出缺氧诱导因子 1α和 AMP 激活的蛋白激酶在这些变化中具有相反的作用。相比之下，抗炎细胞（如 M2 巨噬细胞、调节性 T 细胞和静息记忆 T 细胞）具有较低的糖酵解率和较高的氧化代谢水平。一些抗炎剂可能通过激活 AMP 激活的蛋白激酶诱导类似伪饥饿的状态而起作用。因此，代谢改变可能参与促进或抑制炎症的信号定向程序。
