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The aforementioned outcomes are accomplished through a range of mechanisms, including upregulating the expression of endothelial nitric oxide synthase (eNOS), enhancing the phosphorylation of eNOS at Ser1177, downregulating the expression of NADPH oxidase (NOX), increasing the levels of tetrahydrobiopterin (BH4) in the vasculature through GCH1-dependent pathways, and restoring the coupling of eNOS to facilitate the availability of NO (105)

doi: 10.1021/acsomega.9b04390, 139

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