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

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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