高氧
代谢组
谷氨酰胺
活性氧
氧毒性
转录组
谷胱甘肽
生物
化学
药理学
细胞生物学
生物化学
肺
医学
内科学
酶
基因表达
基因
氨基酸
代谢物
作者
Hao Qin,Wei Zhuang,Xiucheng Liu,Junqi Wu,Shenghui Li,Yan Wang,Xiangming Liu,Chang Chen,Hao Zhang
出处
期刊:Cell Reports
[Elsevier]
日期:2023-07-01
卷期号:42 (7): 112745-112745
被引量:1
标识
DOI:10.1016/j.celrep.2023.112745
摘要
Although increasing evidence suggests potential iatrogenic injury from supplemental oxygen therapy, significant exposure to hyperoxia in critically ill patients is inevitable. This study shows that hyperoxia causes lung injury in a time- and dose-dependent manner. In addition, prolonged inspiration of oxygen at concentrations higher than 80% is found to cause redox imbalance and impair alveolar microvascular structure. Knockout of C-X-C motif chemokine receptor 1 (Cxcr1) inhibits the release of reactive oxygen species (ROS) from neutrophils and synergistically enhances the ability of endothelial cells to eliminate ROS. We also combine transcriptome, proteome, and metabolome analysis and find that CXCR1 knockdown promotes glutamine metabolism and leads to reduced glutathione by upregulating the expression of malic enzyme 1. This preclinical evidence suggests that a conservative oxygen strategy should be recommended and indicates that targeting CXCR1 has the potential to restore redox homeostasis by reducing oxygen toxicity when inspiratory hyperoxia treatment is necessary.
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