Asymmetric Dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) production. ADMA is
generated from methylation of arginine residues by protein arginine methyltransferases (PRMTs) and subsequent proteolysis,
while its elimination is achieved mainly by degradation with dimethylarginine dimethylaminohydrolase (DDAH).
Oxidative stress, endothelial nitric oxide synthase (eNOS) inhibition, eNOS uncoupling, inflammation and shear stress
play a pivotal role in ADMA pathophysiology by managing PRMT/DDAH expression and NO synthesis and leading to a
common result - endothelial dysfunction. Endothelial dysfunction seems to be the common finding in studies investigating
the role of ADMA in cardiovascular disease (CVD). High-performance liquid chromatography (HPLC), mass spectrometry
(MS) and enzyme-linked immunosorbent assay (ELISA) are the existing methods for ADMA quantification. However,
none of them fulfils all the criteria to be characterized as “gold standard”. ADMA is significantly associated with risk factors
for CVD and almost with every disease of the cardiovascular system; showing an independent, strong prognostic
value for mortality and future cardiovascular events. This article aims to review the current knowledge about ADMA biology
and metabolism, pathophysiological mechanisms implicating ADMA in CVD, methods for the determination of
ADMA and its association with CVD risk factors and established CVDs.
Keywords: ADMA, asymmetric dimethylarginine, biomarker, cardiovascular disease, coronary artery disease, heart failure,
hypertension, diabetes mellitus
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