Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/15260
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dc.contributor.authorWattanapitayakul S.K.
dc.contributor.authorBauer J.A.
dc.date.accessioned2021-04-05T04:33:13Z-
dc.date.available2021-04-05T04:33:13Z-
dc.date.issued2001
dc.identifier.issn1637258
dc.identifier.other2-s2.0-0035055046
dc.identifier.urihttps://ir.swu.ac.th/jspui/handle/123456789/15260-
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-0035055046&doi=10.1016%2fS0163-7258%2800%2900114-5&partnerID=40&md5=6b2d6702da4d48164f7937bbb8dbf015
dc.description.abstractDespite some recent declines, cardiovascular disease (CVD) remains the major cause of death in the United States and worldwide. Most recent advances in the treatment of CVD states have been produced by inhibition of mechanisms involved in disease progress. Many studies conducted in the last decade have illustrated increased biological oxidative pathways during CVD in animals and humans. Thus, increased production of reactive oxygen species may be a unifying mechanism in CVD progression, and antioxidants may have therapeutic value in this setting. In this review we address the following questions: Do oxidative mechanisms play a role in CVD? Where do the oxidants come from? What are the relevant oxidative events? What are the therapeutic implications? © 2001 Elsevier Science Inc.
dc.subjectalpha tocopherol
dc.subjectantioxidant
dc.subjectarginine
dc.subjectascorbic acid
dc.subjectbeta carotene
dc.subjectcolestipol
dc.subjectcytokine
dc.subjectfatty acid
dc.subjectglutathione
dc.subjectlipoprotein
dc.subjectnicotinic acid
dc.subjectnitric oxide
dc.subjectnitric oxide synthase
dc.subjectreactive oxygen metabolite
dc.subjectreduced nicotinamide adenine dinucleotide dehydrogenase
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase
dc.subjectretinol
dc.subjectretinol palmitate
dc.subjectsuperoxide dismutase
dc.subjectxanthine oxidase
dc.subjectapoptosis
dc.subjectcalcium signaling
dc.subjectcardiovascular disease
dc.subjectcause of death
dc.subjectcell death
dc.subjectcell infiltration
dc.subjectcoronary artery disease
dc.subjectdisease course
dc.subjectelectron transport
dc.subjectgene expression
dc.subjectheart failure
dc.subjectheart infarction
dc.subjectheart muscle necrosis
dc.subjecthuman
dc.subjecthypertension
dc.subjectlipid metabolism
dc.subjectmitochondrial respiration
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectprotein metabolism
dc.subjectprotein phosphorylation
dc.subjectreview
dc.subjectsignal transduction
dc.subjecttreatment outcome
dc.subjectvitamin supplementation
dc.subjectAnimals
dc.subjectAntioxidants
dc.subjectCardiovascular Diseases
dc.subjectCell Death
dc.subjectDietary Supplements
dc.subjectHumans
dc.subjectNitric Oxide
dc.subjectOxidants
dc.subjectReactive Oxygen Species
dc.titleOxidative pathways in cardiovascular disease: Roles, mechanisms, and therapeutic implications
dc.typeReview
dc.rights.holderScopus
dc.identifier.bibliograpycitationPharmacology and Therapeutics. Vol 89, No.2 (2001), p.187-206
dc.identifier.doi10.1016/S0163-7258(00)00114-5
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