Vohwinkel Christine U, Hoegl Sandra, Eltzschig Holger K
Organ Protection Program, Department of Anesthesiology, University of Colorado School of Medicine, Aurora, Colorado; Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado; and
Organ Protection Program, Department of Anesthesiology, University of Colorado School of Medicine, Aurora, Colorado; Department of Anesthesiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
J Appl Physiol (1985). 2015 Nov 15;119(10):1157-63. doi: 10.1152/japplphysiol.00226.2015. Epub 2015 May 14.
Acute lung injury (ALI) is an inflammatory lung disease that manifests itself in patients as acute respiratory distress syndrome and thereby contributes significantly to the morbidity and mortality of patients experiencing critical illness. Even though it may seem counterintuitive, as the lungs are typically well-oxygenated organs, hypoxia signaling pathways have recently been implicated in the resolution of ALI. For example, functional studies suggest that transcriptional responses under the control of the hypoxia-inducible factor (HIF) are critical in optimizing alveolar epithelial carbohydrate metabolism, and thereby dampen lung inflammation during ALI. In the present review we discuss functional roles of oxygenation, hypoxia and HIFs during ALI, mechanisms of how HIFs are stabilized during lung inflammation, and how HIFs can mediate lung protection during ALI.
急性肺损伤（ALI）是一种炎症性肺部疾病，在患者中表现为急性呼吸窘迫综合征，从而显著增加危重症患者的发病率和死亡率。尽管这可能看似有悖常理，因为肺部通常是氧合良好的器官，但缺氧信号通路最近已被证明与ALI的缓解有关。例如，功能研究表明，在缺氧诱导因子（HIF）控制下的转录反应对于优化肺泡上皮碳水化合物代谢至关重要，从而在ALI期间减轻肺部炎症。在本综述中，我们讨论了ALI期间氧合、缺氧和HIF的功能作用，HIF在肺部炎症期间如何被稳定的机制，以及HIF如何在ALI期间介导肺保护作用。
