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Open AccessEditorial
Int. J. Mol. Sci. 2013, 14(12), 24412-24421;

Biological Functional Relevance of Asymmetric Dimethylarginine (ADMA) in Cardiovascular Disease

Department of Medicine and Science of Aging, University G. D'Annunzio-Chieti, Chieti 66100, Italy
Intensive Cardiology Care Unit, San Camillo de Lellis Hospital, San Severo (FG) 71016, Italy
Author to whom correspondence should be addressed.
Received: 29 October 2013 / Revised: 5 December 2013 / Accepted: 6 December 2013 / Published: 16 December 2013
(This article belongs to the Special Issue ADMA and Nitrergic System)
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Note: In lieu of an abstract, this is an excerpt from the first page.


There is growing evidence that increased levels of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) may contribute to endothelial dysfunction. Studies in animal models as well as in humans have suggested that the increase in ADMA occurs at a time when vascular disease has not yet become clinically evident. ADMA competitively inhibits NO elaboration by displacing L-arginine from NO synthase. In a concentration-dependent manner, it thereby interferes not only with endothelium-dependent, NO-mediated vasodilation, but also with other biological functions exerted by NO. The upshot may be a pro-atherogenic state. Recently, several studies have investigated the effect of various therapeutical interventions on ADMA plasma concentrations. [...] View Full-Text
Keywords: ADMA; nitric oxide; cardiovascular disease ADMA; nitric oxide; cardiovascular disease
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Franceschelli, S.; Ferrone, A.; Pesce, M.; Riccioni, G.; Speranza, L. Biological Functional Relevance of Asymmetric Dimethylarginine (ADMA) in Cardiovascular Disease. Int. J. Mol. Sci. 2013, 14, 24412-24421.

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