Implication of eNOS Uncoupling in Cardiovascular Disease
Keywords:
Cardiovascular disease, eNOS uncoupling, Nitric oxide, Oxidative stress, Reactive oxygen speciesAbstract
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.
Downloads
Published
How to Cite
Issue
Section
License
Submission of an original manuscript to the Journal will be taken to mean that it represents original work not previously published; that it is not being considered elsewhere for publication; that the author(s) agrees to assign copyright to the Journal upon acceptance for publication in the Journal, and if accepted for publication, it will be published in the digital format (PDF) and/or in print and it will not be published elsewhere in the same form, for commercial purposes, in any language, without the consent of the Publisher.