Sites of inflammation are defined by significant changes in metabolic activity. Recent studies have suggested that O2 metabolism and hypoxia play a prominent role in inflammation so-called "inflammatory hypoxia," which results from a combination of recruited inflammatory cells (e.g., neutrophils and monocytes), the local proliferation of multiple cell types, and the activation of multiple O2-consuming enzymes during inflammation. These shifts in energy supply and demand result in localized regions of hypoxia and have revealed the important function off the transcription factor HIF (hypoxia-inducible factor) in the regulation of key target genes that promote inflammatory resolution. Analysis of these pathways has provided multiple opportunities for understanding basic mechanisms of inflammation and has defined new targets for intervention. Here, we review recent work addressing tissue hypoxia and metabolic control of inflammation and immunity.

中文翻译：

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缺氧和粘膜炎症。

炎症部位由代谢活性的显着变化定义。最近的研究表明，氧气代谢和缺氧在炎症中起着重要作用，所谓的“炎症性缺氧”是由募集的炎症细胞（例如嗜中性粒细胞和单核细胞），多种细胞类型的局部增殖以及在炎症过程中激活多种消耗氧气的酶。能量供需的这些变化导致局部缺氧，并揭示了转录因子HIF（低氧诱导因子）在调节促进炎症消退的关键靶基因中的重要功能。对这些途径的分析为理解炎症的基本机制提供了多种机会，并确定了新的干预目标。