4.7 Editorial Material

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

Journal

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 14, Issue 12, Pages 24412-24421

Publisher

MDPI
DOI: 10.3390/ijms141224412

Keywords

ADMA; nitric oxide; cardiovascular disease

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available