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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/75251
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dc.contributor.authorGaiolla, Paula Schmidt Azevedo-
dc.contributor.authorMinicucci, Marcos Ferreira-
dc.contributor.authorSantos, Priscila P.-
dc.contributor.authorPaiva, Sergio Alberto Rupp de-
dc.contributor.authorZornoff, Leonardo Antonio Mamede-
dc.date.accessioned2014-05-27T11:29:02Z-
dc.date.accessioned2016-10-25T18:48:00Z-
dc.date.available2014-05-27T11:29:02Z-
dc.date.available2016-10-25T18:48:00Z-
dc.date.issued2013-05-01-
dc.identifierhttp://dx.doi.org/10.1097/CRD.0b013e318274956d-
dc.identifier.citationCardiology in Review, v. 21, n. 3, p. 135-140, 2013.-
dc.identifier.issn1061-5377-
dc.identifier.issn1538-4683-
dc.identifier.urihttp://hdl.handle.net/11449/75251-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/75251-
dc.description.abstractFatty acids are the main substrates used by mitochondria to provide myocardial energy under normal conditions. During heart remodeling, however, the fuel preference switches to glucose. In the earlier stages of cardiac remodeling, changes in energy metabolism are considered crucial to protect the heart from irreversible damage. Furthermore, low fatty acid oxidation and the stimulus for glycolytic pathway lead to lipotoxicity, acidosis, and low adenosine triphosphate production. While myocardial function is directly associated with energy metabolism, the metabolic pathways could be potential targets for therapy in heart failure. © 2013 by Lippincott Williams & Wilkins.en
dc.format.extent135-140-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectβ-oxidation-
dc.subjectcardiac failure-
dc.subjectenergy metabolism-
dc.subjectglycolysis-
dc.subjectheart remodeling-
dc.subjectmitochondrial dysfunction-
dc.subjectadenosine triphosphate-
dc.subjectglucose transporter 1-
dc.subjectglucose transporter 4-
dc.subjectlactate dehydrogenase-
dc.subjectprotein kinase B-
dc.subjectranolazine-
dc.subjectbioavailability-
dc.subjectcarbohydrate metabolism-
dc.subjectcell damage-
dc.subjectcitric acid cycle-
dc.subjectenergy yield-
dc.subjectesterification-
dc.subjectfatty acid oxidation-
dc.subjectglucose oxidation-
dc.subjectglucose transport-
dc.subjectheart failure-
dc.subjectheart function-
dc.subjectheart muscle metabolism-
dc.subjectheart ventricle remodeling-
dc.subjecthuman-
dc.subjectlipid storage-
dc.subjectlipotoxicity-
dc.subjectmetabolism-
dc.subjectmitochondrial dynamics-
dc.subjectmitochondrial membrane-
dc.subjectoxidative phosphorylation-
dc.subjectoxidative stress-
dc.subjectoxygen consumption-
dc.subjectprotein dephosphorylation-
dc.subjectrespiratory chain-
dc.subjectreview-
dc.subjectsarcoplasmic reticulum-
dc.subjectupregulation-
dc.subjectAdenosine Triphosphate-
dc.subjectChronic Disease-
dc.subjectEnergy Metabolism-
dc.subjectHeart-
dc.subjectHeart Failure-
dc.subjectHumans-
dc.subjectMitochondria, Heart-
dc.subjectMitochondrial Diseases-
dc.subjectMyocardium-
dc.subjectNitric Oxide-
dc.subjectOxidation-Reduction-
dc.titleEnergy Metabolism in Cardiac Remodeling and Heart Failureen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionFaculdade de Medicina-
dc.description.affiliationInternal Medicine Department Botucatu Medical School UNESP-São Paulo State University, CEP 18618-970, Sao Paulo-
dc.description.affiliationDepartamento de Clínica Médica Faculdade de Medicina, Botucatu Rubião Júnior s/n, Botucatu, Sao Paulo-
dc.description.affiliationUnespInternal Medicine Department Botucatu Medical School UNESP-São Paulo State University, CEP 18618-970, Sao Paulo-
dc.identifier.doi10.1097/CRD.0b013e318274956d-
dc.identifier.wosWOS:000317590000004-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofCardiology in Review-
dc.identifier.scopus2-s2.0-84876408688-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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