6533b839fe1ef96bd12a5c73
RESEARCH PRODUCT
Vascular oxidative stress, nitric oxide and atherosclerosis.
Huige LiUlrich FörstermannSven Horkesubject
Xanthine OxidaseAntioxidantNitric Oxide Synthase Type IIImedicine.medical_treatmentMice TransgenicOxidative phosphorylationNitric Oxide Synthase Type Imedicine.disease_causeNitric OxideCardiovascular SystemAntioxidantsNitric oxideSuperoxide dismutasechemistry.chemical_compoundMiceSuperoxidesmedicineAnimalsHumansXanthine oxidasechemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseNADPH oxidasebiologyAryldialkylphosphataseSuperoxide DismutaseNADPH OxidasesAtherosclerosisCatalaseMitochondriaOxidative StresschemistryBiochemistrybiology.proteinCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressdescription
In the vascular wall, reactive oxygen species (ROS) are produced by several enzyme systems including NADPH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase (eNOS) and the mitochondrial electron transport chain. On the other hand, the vasculature is protected by antioxidant enzyme systems, including superoxide dismutases, catalase, glutathione peroxidases and paraoxonases, which detoxify ROS. Cardiovascular risk factors such as hypercholesterolemia, hypertension, and diabetes mellitus enhance ROS generation, resulting in oxidative stress. This leads to oxidative modification of lipoproteins and phospholipids, mechanisms that contribute to atherogenesis. In addition, oxidation of tetrahydrobiopterin may cause eNOS uncoupling and thus potentiation of oxidative stress and reduction of eNOS-derived NO, which is a protective principle in the vasculature. This review summarizes the latest advances in the role of ROS-producing enzymes, antioxidative enzymes as well as NO synthases in the initiation and development of atherosclerosis.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2014-11-01 | Atherosclerosis |