Source:http://linkedlifedata.com/resource/pubmed/id/20477274
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2010-5-18
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pubmed:abstractText |
Acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS) are common and important stages of both pulmonary and systemic critical illnesses. ALI/ARDS is categorized as primary or secondary based on the etiology of the disease. There is increasing evidence to suggest the involvement of airway epithelial cells in the pathogenesis of ALI/ARDS. The airway epithelial cell is a new candidate as a biological target responsible for development of the disease and the role of these cells in the pathogenesis of ALI/ARDS is under investigation. This review describes the importance of the airway epithelial cell in the development of ALI/ARDS, its role as the first line of lung defense facing local and primary challenges, its role as an important player in the development of airway inflammation and remodeling, as an inflammatory promoter for initiating both local and systemic inflammation and as an active producer of several inflammatory and anti-inflammatory mediators. It is hypothesized that airway epithelial cells may contribute to ALI/ARDS via Toll-like receptor-involved mediators, reactive oxygen species-involved reactions and an imbalance between protease and antiprotease activation. The airway epithelial cell may be a valuable therapeutic target for discovering and developing new drugs and/or new therapeutic strategies for ALI/ARDS.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:status |
PubMed-not-MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1747-6356
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
149-55
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pubmed:year |
2007
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pubmed:articleTitle |
Airway epithelial dysfunction in the development of acute lung injury and acute respiratory distress syndrome.
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pubmed:affiliation |
Fudan University, Department of Pulmonary Medicine, Zhongshan Hospital, 180 Feng Lin Road, Shanghai 200032, PR China. xiangdong.wang@telia.com
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pubmed:publicationType |
Journal Article
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