Journal article

Abstract 220: Regulation of Dimethylamine Dimethylaminohydrolase in the Liver

Amy L Wilson-O'Brien, John Garlick, Andrew M Wilson

Arteriosclerosis, Thrombosis, and Vascular Biology | Ovid Technologies (Wolters Kluwer Health) | Published : 2016


Introduction: Nitric Oxide (NO) is a crucial molecule in cardiovascular biology. Abnormalities in NO are critical in atherosclerosis and impairment of the NO pathway increases risk of cardiovascular disease (CVD). A possible cause of endothelial dysfunction is an elevation (in plasma) of the endogenous inhibitor of NO synthase, asymmetric dimethylarginine (ADMA). ADMA was initially described in renal failure. 80% of ADMA is metabolized by the enzyme dimethylarginine dimethylaminohydrolase (DDAH) in the liver. DDAH-1 is widely distributed and felt to be the major determinant of circulating ADMA levels. Very little data is available regarding the cause and effects of DDAH dysregula..

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