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BioMed Research International
Volume 2014 (2014), Article ID 501612, 11 pages
Review Article

The Endothelial ADMA/NO Pathway in Hypoxia-Related Chronic Respiratory Diseases

1University Medical Center Hamburg-Eppendorf, Department of Clinical Pharmacology and Toxicology, Martinistraße 52, 20246 Hamburg, Germany
2University Medical Center Hamburg-Eppendorf, II Department of Medicine-Oncology, Hematology, Stem Cell Transplantation, Section of Pneumology, Hamburg, Germany
3The Vera Moulton Wall Center for Pulmonary Vascular Disease and Cardiovascular Institute, Stanford University - School of Medicine, Stanford, USA

Received 14 November 2013; Accepted 18 January 2014; Published 25 February 2014

Academic Editor: Silvia M. Arribas

Copyright © 2014 Nicole Lüneburg et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Since its discovery, many adhere to the view that asymmetric dimethylarginine (ADMA), as an inhibitor of the synthesis of nitric oxide (NO), contributes to the pathogenesis of various diseases. Particularly, this is evident in disease of the cardiovascular system, in which endothelial dysfunction results in an imbalance between vasoconstriction and vasodilatation. Even if increased ADMA concentrations are closely related to an endothelial dysfunction, several studies pointed to a potential beneficial effect of ADMA, mainly in the context of angioproliferative disease such as cancer and fibrosis. Antiproliferative properties of ADMA independent of NO have been identified in this context. In particular, the regulation of ADMA by its degrading enzyme dimethylarginine dimethylaminohydrolase (DDAH) is the object of many studies. DDAH is discussed as a promising therapeutic target for the indirect regulation of NO. In hypoxia-related chronic respiratory diseases, this controversy discussion of ADMA and DDAH is particularly evident and is therefore subject of this review.