Endothelial Dysfunction Due to eNOS Uncoupling: Molecular Mechanisms as Potential Therapeutic Targets

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The authors discuss the main mechanisms of endothelial nitric oxide synthase (eNOS) uncoupling, including oxidative depletion of the critical eNOS cofactor BH4, deficiency of eNOS substrate L-Arg, or accumulation of its analog asymmetrical dimethylarginine, and eNOS S-glutathionylation.
[Cellular & Molecular Biology Letters]
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