Hypoxia and Reoxygenation Induce Endothelial Nitric Oxide Synthase Uncoupling in Endothelial Cells through Tetrahydrobiopterin Depletion and S-Glutathionylation

@inproceedings{Pascali2014HypoxiaAR,
  title={Hypoxia and Reoxygenation
Induce Endothelial Nitric
Oxide Synthase Uncoupling in Endothelial Cells through Tetrahydrobiopterin
Depletion and S-Glutathionylation},
  author={Francesco De Pascali and Craig F. Hemann and Kindra Samons and Chun-An Chen and Jay L. Zweier},
  booktitle={Biochemistry},
  year={2014}
}
Ischemia-reperfusion injury is accompanied by endothelial hypoxia and reoxygenation that trigger oxidative stress with enhanced superoxide generation and diminished nitric oxide (NO) production leading to endothelial dysfunction. Oxidative depletion of the endothelial NO synthase (eNOS) cofactor tetrahydrobiopterin can trigger eNOS uncoupling, in which the enzyme generates superoxide rather than NO. Recently, it has also been shown that oxidative stress can induce eNOS S-glutathionylation at… CONTINUE READING

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