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高氧诱导急性肺损伤的分子机制

Molecular mechanisms of hyperoxia-induced acute lung injury.

作者信息

Bhandari Vineet

机构信息

Division of Perinatal Medicine, Yale University School of Medicine, Department of Pediatrics, 333 Cedar Street, LCI 401B, New Haven, CT 06520-8064, USA.

出版信息

Front Biosci. 2008 May 1;13:6653-61. doi: 10.2741/3179.

DOI:10.2741/3179
PMID:18508685
Abstract

Hyperoxia-induced acute lung injury (HALI) is characterized by an influx of inflammatory cells, increased pulmonary permeability, endothelial and epithelial cell death. Reactive oxygen species have been postulated to have a significant role in HALI, in part, by inducing cell death responses regulated by shared common mediators of apoptotic and necrotic pathways. Significant differences exist in the response of the mature and developing lung to HALI.

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。活性氧被认为在HALI中起重要作用,部分原因是通过诱导由凋亡和坏死途径的共同介质调节的细胞死亡反应。成熟肺和发育中肺对HALI的反应存在显著差异。

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