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Combined with the concurrent upregulation of dimethylargininase, which degrades an inhibitor of nitric oxide synthase, has been associated with augmented neovascularization, and was overexpressed 1.5-fold (p=0.002) in semaglutide-treated animals, this constitutes substantial evidence of the relevance of the nitric oxide biosynthetic pathway to an account of the cardiac effects of semaglutide

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