Implication of eNOS Uncoupling in Cardiovascular Disease

Authors

  • Ning Xia Department of Pharmacology, Johannes Gutenberg University Medical Center, Mainz, Germany
  • Ulrich Förstermann Department of Pharmacology, Johannes Gutenberg University Medical Center, Mainz, Germany
  • Huige Li Department of Pharmacology, Johannes Gutenberg University Medical Center, Mainz, Germany; Center for Translational Vascular Biology (CTVB), Johannes Gutenberg University Medical Center, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany http://orcid.org/0000-0003-3458-7391

Keywords:

Cardiovascular disease, eNOS uncoupling, Nitric oxide, Oxidative stress, Reactive oxygen species

Abstract

Under physiological conditions, nitric oxide (NO) is produced in the vasculature mainly by the endothelial nitric oxide synthase (eNOS). Endothelial NO relaxes blood vessels, inhibits platelet activity, and protects against atherosclerosis. Under pathological conditions such as hypertension, diabetes, and hypercholesterolemia, eNOS may become uncoupled. Uncoupled eNOS generates superoxide at the expense of NO and contributes substantially to oxidative stress and endothelial dysfunction. Major mechanisms of eNOS uncoupling include deficiency of the eNOS cofactor tetrahydrobiopterin, deficiency of the eNOS substrate L-arginine, and eNOS S-glutathionylation. Reversal of eNOS uncoupling may represent a feasible strategy for the prevention and treatment of cardiovascular diseases.

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Published

2017-01-01

How to Cite

Xia, N., Förstermann, U., & Li, H. (2017). Implication of eNOS Uncoupling in Cardiovascular Disease. Reactive Oxygen Species, 3(7), 38–46. Retrieved from https://rosj.org/index.php/ros/article/view/70

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