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血管生成素2在高氧诱导的急性肺损伤中的作用。

The role of angiopoietin 2 in hyperoxia-induced acute lung injury.

作者信息

Bhandari Vineet, Elias Jack A

机构信息

Divison of Perinatal Medicine, Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut, USA.

出版信息

Cell Cycle. 2007 May 2;6(9):1049-52. doi: 10.4161/cc.6.9.4229.

DOI:10.4161/cc.6.9.4229
PMID:17438375
Abstract

Hyperoxia-induced acute lung injury (HALI) is characterized by an influx of inflammatory cells, increased pulmonary permeability, endothelial and epithelial cell death. In a murine model and in vitro, we found Angiopoietin 2 to be a critical mediator of lung oxidant injury, inflammation, edema, and regulator of necrotic cell death pathways. The clinical significance of our findings was highlighted by the detection of increased Angiopoietin 2 levels in patients with ALI.

摘要

高氧诱导的急性肺损伤(HALI)的特征是炎症细胞流入、肺通透性增加、内皮细胞和上皮细胞死亡。在小鼠模型和体外实验中,我们发现血管生成素2是肺氧化损伤、炎症、水肿的关键介质,也是坏死细胞死亡途径的调节因子。急性肺损伤(ALI)患者血管生成素2水平升高的检测突出了我们研究结果的临床意义。

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