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dc.contributor.authorBajic, Vladan P.
dc.contributor.authorVan Neste, Christophe Marc
dc.contributor.authorObradovic, Milan
dc.contributor.authorZafirovic, Sonja
dc.contributor.authorRadak, Djordje
dc.contributor.authorBajic, Vladimir B.
dc.contributor.authorEssack, Magbubah
dc.contributor.authorIsenovic, Esma R.
dc.date.accessioned2019-05-14T12:53:04Z
dc.date.available2019-05-14T12:53:04Z
dc.date.issued2019-05-09
dc.identifier.citationBajic VP, Van Neste C, Obradovic M, Zafirovic S, Radak D, et al. (2019) Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease. Oxidative Medicine and Cellular Longevity 2019: 1–14. Available: http://dx.doi.org/10.1155/2019/5028181.
dc.identifier.issn1942-0900
dc.identifier.issn1942-0994
dc.identifier.doi10.1155/2019/5028181
dc.identifier.urihttp://hdl.handle.net/10754/652879
dc.description.abstractMore people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired “redox homeostasis,” which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.
dc.description.sponsorshipThis work has been supported by grants from the Ministry of Education, Science and Technological Development, Republic of Serbia (No. 173033 (ERI), No. 173034 (BSP), and No. 41002 (DjR)). VBB has been supported by the King Abdullah University of Science and Technology (KAUST) Base Research Fund (BAS/1/1606-01-01) and ME by KAUST Office of Sponsored Research (OSR) Awards (No. FCC/1/1976-24-01).
dc.publisherHindawi Limited
dc.relation.urlhttps://www.hindawi.com/journals/omcl/2019/5028181/
dc.rightsThis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.titleGlutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease
dc.typeArticle
dc.contributor.departmentComputer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
dc.contributor.departmentApplied Mathematics and Computational Science Program
dc.contributor.departmentComputational Bioscience Research Center (CBRC)
dc.identifier.journalOxidative Medicine and Cellular Longevity
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionLaboratory for Radiobiology and Molecular Genetics, Institute of Nuclear Sciences Vinca, University of Belgrade, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia
dc.contributor.institutionDepartment of Vascular Surgery, Dedinje Cardiovascular Institute, Belgrade University School of Medicine, Belgrade, Serbia
kaust.personVan Neste, Christophe Marc
kaust.personBajic, Vladimir B.
kaust.personEssack, Magbubah
kaust.grant.numberBAS/1/1606-01-01
kaust.grant.numberFCC/1/1976-24-01
refterms.dateFOA2019-05-14T13:04:48Z


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This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.