Sepsis is a highly heterogeneous syndrome that is caused by an imbalanced host response to infection. Despite huge investments, sepsis remains a contemporary threat with significant burden on health systems. Vascular dysfunction and elevated oxygen consumption by highly metabolically active immune cells result in tissue hypoxia during inflammation. The transcription factor hypoxia-inducible factor-1a (HIF1α), and its family members, plays an important role in cellular metabolism and adaptation to cellular stress caused by hypoxia. In this review, we discuss the role of HIF in sepsis. We show possible mechanisms by which the inflammatory response activated during sepsis affects the HIF pathway. The activated HIF pathway in turn changes the metabolism of both innate and adaptive immune cells. As HIF expression in leukocytes of septic patients can be directly linked with mortality, we discuss multiple ways of interfering with the HIF signaling pathway.

中文翻译：

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败血症期间代谢重编程中的缺氧诱导因子。

脓毒症是高度异质性综合症，是由宿主对感染的反应不平衡引起的。尽管投入了大量资金，败血症仍然是当今的威胁，给卫生系统带来了沉重负担。高度代谢活跃的免疫细胞的血管功能障碍和耗氧量增加，导致炎症期间组织缺氧。转录因子缺氧诱导因子-1a（HIF1α）及其家族成员在细胞代谢和适应由缺氧引起的细胞应激中起重要作用。在这篇综述中，我们讨论了HIF在败血症中的作用。我们显示了败血症期间激活的炎症反应影响HIF途径的可能机制。激活的HIF途径进而改变先天和适应性免疫细胞的代谢。