Abstract
Background and Aims: Atherosclerosis is a chronic inflammatory disease characterised by the build-up of arterial lipid plaques. M1 macrophages have a crucial role in progression and pathogenesis of atherosclerosis. Dimethylarginine dimethylaminohydrolase (DDAH) enzymes metabolise the endogenous nitric oxide synthase (NOS) inhibitor, asymmetric dimethylarginine (ADMA), an independent risk factor for atherosclerosis. Two isoforms are known for DDAH, each with distinct tissue specificity. In mice atherosclerotic models, DDAH-1 overexpression reduced plaque formation through ADMA.
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