Abstract
In the airways, arginase and NOS compete for the common substrate L-arginine. In chronic airway diseases, such as asthma and COPD, elevated arginase expression contributes to airway contractility, hyperresponsiveness, inflammation and remodeling. The disrupted L-arginine homeostasis, through changes in arginase and NOS expression and activity, does not only play a central role in the development of various airways diseases such as asthma or COPD. It possibly also affects L-arginine homeostasis throughout the body contributing to the emergence of co-morbidities. This review focusses on the role of arginase, NOS and ADMA in co-morbidities of asthma and COPD and speculates on their possible connection.
Original language | English |
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Pages (from-to) | 126-133 |
Number of pages | 8 |
Journal | Current Opinion in Pharmacology |
Volume | 40 |
Early online date | 2018 |
DOIs | |
Publication status | Published - Jun-2018 |
Keywords
- OBSTRUCTIVE SLEEP-APNEA
- ASYMMETRIC DIMETHYLARGININE ADMA
- T-CELL RESPONSES
- ARGININE METABOLISM
- PULMONARY-DISEASE
- ATOPIC-DERMATITIS
- ADIPOSE-TISSUE
- DEPRESSED-PATIENTS
- ALLERGIC RHINITIS
- SYNTHASE ACTIVITY