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RESEARCH PRODUCT
Implication of eNOS Uncoupling in Cardiovascular Disease
Huige LiUlrich FörstermannNing Xiasubject
chemistry.chemical_classificationmedicine.medical_specialtyReactive oxygen speciesbiologybusiness.industrySuperoxideTetrahydrobiopterinbiology.organism_classificationmedicine.disease_causemedicine.diseaseNitric oxidechemistry.chemical_compoundEndocrinologychemistryEnosInternal medicinemedicinePlatelet activationEndothelial dysfunctionbusinessOxidative stressmedicine.drugdescription
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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2017-01-01 | Reactive Oxygen Species |