Targeting arginase and nitric oxide metabolism in chronic airway diseases and their co-morbidities

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.