Journal
TRENDS IN MOLECULAR MEDICINE
Volume 11, Issue 11, Pages 481-484Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2005.09.009
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Funding
- NHLBI NIH HHS [R01 HL 59337, R01 HL 69170] Funding Source: Medline
- NIAID NIH HHS [1U19 AI 34607] Funding Source: Medline
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Conventionally, asthma is defined as involving both airway inflammation and airway smooth muscle hyper-responsiveness. However, Que and coworkers have recently uncoupled these concepts, showing that mice lacking an S-nitrosothiol reductase have allergen-induced airway inflammation but do not have airway hyper-responsiveness. These data are consistent with recent clinical evidence that: (i) S-nitrosothiol signaling is abnormal in human asthma, (ii) nitric oxide in exhaled air might be only a biomarker for the metabolism of more physiologically relevant nitrogen oxides and (iii) the biochemical response to airway inflammation is central to asthma pathophysiology.
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