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dc.creatorObradović, Milan M.
dc.creatorZarić, Božidarka
dc.creatorSudar-Milovanović, Emina
dc.creatorPerović, Milan
dc.creatorResanović, Ivana
dc.creatorGluvić, Zoran
dc.creatorIsenović, Esma R.
dc.date.accessioned2019-02-01T12:55:10Z
dc.date.available2019-02-01T12:55:10Z
dc.date.issued2018
dc.identifier.isbn9781536141856; 9781536141849
dc.identifier.urihttps://vinar.vin.bg.ac.rs/handle/123456789/8014
dc.description.abstractNitric oxide (NO) is a free radical which, in reactions with various molecules causes multiple biological effects. NO is exceptionally regulated and extends to almost every cell type and function within circulation. Generation and actions of NO are regulated by various hormones under physiological and pathophysiological conditions. Nitric oxide synthases (NOS) are the enzymes responsible for NO generation. In mammals, neuronal NOS (nNOS) and endothelial NOS (eNOS) are constitutively expressed, while inducible NOS (iNOS) mediate in immune defense. Altered NO level is associated with obesity, insulin resistance (IR), diabetes and cardiovascular diseases (CVD). Disturbances in eNOS and iNOS regulation accompany multiple changes in endothelial function and contribute to development of CVD. Furthermore, key step in initiation and progression of atherosclerosis is reduction in bioactivity of endothelial cell-derived NO. Here we shall focus on recent literature data related to the role of eNOS and iNOS in physiological and pathophysiological conditions. © 2018 Nova Science Publishers, Inc. All rights reserved.en
dc.language.isoen
dc.publisherNova Science Publishers
dc.rightsopenAccess
dc.sourceHorizons in World Cardiovascular Research
dc.subjectCVDen
dc.subjecteNOSen
dc.subjectiNOSen
dc.subjectNOen
dc.titleThe role of eNOS and iNOS in pathophysiological conditionsen
dc.typebookPart
dc.rights.licenseARR
dcterms.abstractИсеновић, Есма Р.; Судар-Миловановић, Емина; Обрадовић, Милан М.; Перовић, Милан; Зарић, Божидарка; Глувић, Зоран; Ресановић, Ивана;
dc.rights.holder© Nova Science Publishers
dc.citation.volume15
dc.citation.spage65
dc.citation.epage102
dc.type.versionpublishedVersion
dc.identifier.scopus2-s2.0-85058918710
dc.identifier.rcubhttps://hdl.handle.net/21.15107/rcub_vinar_8014


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