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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; in revised form: 5 December 2013 / Accepted: 6 December 2013 / Published: 16 December 2013
Abstract: 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.
Keywords: ADMA; nitric oxide; cardiovascular disease
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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.
Franceschelli S, Ferrone A, Pesce M, Riccioni G, Speranza L. Biological Functional Relevance of Asymmetric Dimethylarginine (ADMA) in Cardiovascular Disease. International Journal of Molecular Sciences. 2013; 14(12):24412-24421.
Franceschelli, Sara; Ferrone, Alessio; Pesce, Mirko; Riccioni, Graziano; Speranza, Lorenza. 2013. "Biological Functional Relevance of Asymmetric Dimethylarginine (ADMA) in Cardiovascular Disease." Int. J. Mol. Sci. 14, no. 12: 24412-24421.