6533b85afe1ef96bd12b8a74

RESEARCH PRODUCT

Uncoupling of eNOS in Cardiovascular Disease

Huige LiUlrich Förstermann

subject

0301 basic medicinemedicine.medical_specialtyArgininebiologySuperoxidebusiness.industryNitric Oxide Synthase Type IIITetrahydrobiopterin030204 cardiovascular system & hematologybiology.organism_classificationmedicine.diseaseVasoprotectiveNitric oxide03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicineEndocrinologychemistryEnosInternal medicinemedicineEndothelial dysfunctionbusinessmedicine.drug

description

Abstract Under physiological conditions, nitric oxide (NO) produced by the endothelial NO synthase (eNOS) represents a key vasoprotective factor. Under conditions of cardiovascular diseases, such as hypertension, diabetes, and atherosclerosis, eNOS may become uncoupled. Uncoupled eNOS generates superoxide at the expense of NO and contributes significantly to endothelial dysfunction and atherogenesis. Major mechanisms of eNOS uncoupling include depletion of tetrahydrobiopterin, an essential cofactor for the eNOS enzyme, and deficiency of l -arginine, the eNOS substrate, and/or eNOS S-glutathionylation. Reversal of eNOS uncoupling may represent a novel therapeutic strategy for the prevention and treatment of cardiovascular diseases.

yearjournalcountryeditionlanguage
2017-01-01
https://doi.org/10.1016/b978-0-12-804273-1.00009-0