节点文献

新生儿高氧肺损伤机制研究进展

Recent advances in hyperoxia-induced lung injury in newborn

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 彭琼玲常立文

【Author】 PENG Qiong-ling,CHANG Li-wen(Department of Pediatrics,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,Hubei,China)

【机构】 华中科技大学同济医学院附属同济医院儿科

【摘要】 新生儿高氧肺损伤是一个极其复杂的病理生理过程,其损伤机制涉及炎性水肿、血管生成、细胞外基质重建、组织异常修复和细胞凋亡等多种因素,且这些因素交织成网,相互影响,共同形成了高氧肺损伤的病理特征。文章综述了近年研究较多且在高氧肺损伤病理过程中发挥重要作用的分子系统,包括水通道蛋白、基质金属蛋白酶、血管内皮生长因子、单核细胞趋化因子和细胞凋亡相关因子。

【Abstract】 The pathophysiology of hyperoxia-induced lung injury in the newborns is very complicated.The mechanisms involve inflammatory edema,angiogenesis,extracellular matrix regeneration,abnormal repair of tissues,and apoptosis of cells.These factors affect each other and form the pathological characteristics of this injury.This article reviewed the recent extensively studied molecular systems that have important effects on the process of hyperoxia-induced lung injury,including aquaporins,matrix metalloproteinases,vascular endothelial growth factor,chemokines and apoptosis-associated factors.

  • 【文献出处】 临床儿科杂志 ,Journal of Clinical Pediatrics , 编辑部邮箱 ,2008年06期
  • 【分类号】R722.1
  • 【被引频次】13
  • 【下载频次】329
节点文献中: 

本文链接的文献网络图示:

本文的引文网络