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Curr Opin Pharmacol. 2018 Jun;40:126-133. doi: 10.1016/j.coph.2018.04.010. Epub 2018 May 2.

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

Author information

1
Department of Molecular Pharmacology, University of Groningen, Antonius Deusinglaan 1 (XB10), 9713 AV Groningen, The Netherlands; Groningen Research Institute for Asthma and COPD (GRIAC), University of Groningen, Groningen, The Netherlands.
2
Department of Molecular Pharmacology, University of Groningen, Antonius Deusinglaan 1 (XB10), 9713 AV Groningen, The Netherlands; Groningen Research Institute for Asthma and COPD (GRIAC), University of Groningen, Groningen, The Netherlands. Electronic address: r.gosens@rug.nl.

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.

PMID:
29729549
DOI:
10.1016/j.coph.2018.04.010
[Indexed for MEDLINE]
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