The endothelial ADMA/NO pathway in hypoxia-related chronic respiratory diseases

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The endothelial ADMA/NO pathway in hypoxia-related chronic respiratory diseases. / Lüneburg, Nicole; Harbaum, Lars; Hennigs, Jan K.

In: BIOMED RES INT , Vol. 2014, 01.01.2014, p. 501612.

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@article{cb34306117944b08bb277a786dbc5976,
title = "The endothelial ADMA/NO pathway in hypoxia-related chronic respiratory diseases",
abstract = "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.",
author = "Nicole L{\"u}neburg and Lars Harbaum and Hennigs, {Jan K}",
year = "2014",
month = jan,
day = "1",
doi = "10.1155/2014/501612",
language = "English",
volume = "2014",
pages = "501612",
journal = "BIOMED RES INT ",
issn = "2314-6133",
publisher = "Hindawi Publishing Corporation",

}

RIS

TY - JOUR

T1 - The endothelial ADMA/NO pathway in hypoxia-related chronic respiratory diseases

AU - Lüneburg, Nicole

AU - Harbaum, Lars

AU - Hennigs, Jan K

PY - 2014/1/1

Y1 - 2014/1/1

N2 - 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.

AB - 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.

U2 - 10.1155/2014/501612

DO - 10.1155/2014/501612

M3 - SCORING: Journal article

C2 - 24719871

VL - 2014

SP - 501612

JO - BIOMED RES INT

JF - BIOMED RES INT

SN - 2314-6133

ER -