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Vitamin C prevents stress-induced damage on the heart caused by the death of cardiomyocytes, through down-regulation of the excessive production of catecholamine, TNF-alpha, and ROS production in Gulo (-/-)(Vit C-Insufficient) mice

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dc.contributor.authorKim, Hyemin-
dc.contributor.authorBae, Seyeon-
dc.contributor.authorKim, Yejin-
dc.contributor.authorCho, Chung-Hyun-
dc.contributor.authorKim, Sung Joon-
dc.contributor.authorKim, Yong-Jin-
dc.contributor.authorLee, Seung-Pyo-
dc.contributor.authorKim, Hang-Rae-
dc.contributor.authorHwang, Young-il-
dc.contributor.authorKang, Jae Seung-
dc.contributor.authorLee, Wang Jae-
dc.date.accessioned2024-05-16T01:32:30Z-
dc.date.available2024-05-16T01:32:30Z-
dc.date.created2020-12-02-
dc.date.created2020-12-02-
dc.date.created2020-12-02-
dc.date.created2020-12-02-
dc.date.issued2013-12-
dc.identifier.citationFree Radical Biology and Medicine, Vol.65, pp.573-583-
dc.identifier.issn0891-5849-
dc.identifier.urihttps://hdl.handle.net/10371/202652-
dc.description.abstractIt is thought that vitamin C has protective roles on stress-induced heart damage and the development of cardiovascular diseases, but its precise role and mechanisms are unclear. In the present study, we investigated the specific mechanisms by which vitamin C leads to protecting the heart from stress-induced damage in the Gulo(-/-) mice which cannot synthesize vitamin C like humans. By exposure to stress (1 h/day), the heartbeat and cardiac output in vitamin C-insufficient Gulo(-/-) mice were definitely decreased, despite a significant increase of adrenaline (ADR) and noradrenaline (NA) production. A change of cardiac structure caused by the death of cardiomyocytes and an increased expression of matrix metalloprotease (MMP)-2 and -9 were also found. Moreover, lipid peroxidation and the production of tumor necrosis factor-alpha (TNF-alpha) in the heart were increased. Finally, all vitamin C-insufficient Gulo(-/-) mice were expired within 2 weeks. Interestingly, all of the findings in vitamin C-insufficient Gulo(-/-) mice were completely prevented by the supplementation of a sufficient amount of vitamin C. Taken together, vitamin C insufficiency increases the risk of stress-induced cardiac damage with structural and functional changes arising from the apoptosis of cardiomyocytes. Crown Copyright (C) 2013 Published by Elsevier Inc. All rights reserved.-
dc.language영어-
dc.publisherElsevier BV-
dc.titleVitamin C prevents stress-induced damage on the heart caused by the death of cardiomyocytes, through down-regulation of the excessive production of catecholamine, TNF-alpha, and ROS production in Gulo (-/-)(Vit C-Insufficient) mice-
dc.typeArticle-
dc.identifier.doi10.1016/j.freeradbiomed.2013.07.023-
dc.citation.journaltitleFree Radical Biology and Medicine-
dc.identifier.wosid000328868900055-
dc.identifier.scopusid2-s2.0-84884528684-
dc.citation.endpage583-
dc.citation.startpage573-
dc.citation.volume65-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorCho, Chung-Hyun-
dc.contributor.affiliatedAuthorKim, Sung Joon-
dc.contributor.affiliatedAuthorKim, Yong-Jin-
dc.contributor.affiliatedAuthorKim, Hang-Rae-
dc.contributor.affiliatedAuthorHwang, Young-il-
dc.contributor.affiliatedAuthorKang, Jae Seung-
dc.contributor.affiliatedAuthorLee, Wang Jae-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusTUMOR-NECROSIS-FACTOR-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusASCORBIC-ACID-
dc.subject.keywordPlusSIGNALING PATHWAYS-
dc.subject.keywordPlusCARDIOVASCULAR-DISEASE-
dc.subject.keywordPlusLIPID-PEROXIDATION-
dc.subject.keywordPlusCARDIAC MYOCYTES-
dc.subject.keywordPlusFAILURE-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusOXYGEN-
dc.subject.keywordAuthorVitamin C insufficiency-
dc.subject.keywordAuthorGulo(-/-) mice-
dc.subject.keywordAuthorStress-
dc.subject.keywordAuthorHeart injury-
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