Role of beta-adrenergic receptors and sirtuin signaling in the heart during aging, heart failure, and adaptation to stress

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dc.citation.issue1
dc.citation.volume38
dc.contributor.authorSpadari, Regina Celia [UNIFESP]
dc.contributor.authorCavadas, Claudia
dc.contributor.authorCarvalho, Ana Elisa Teofilo Saturi de [UNIFESP]
dc.contributor.authorOrtolani, Daniela [UNIFESP]
dc.contributor.authorMoura, Andre Luiz de [UNIFESP]
dc.contributor.authorVassallo, Paula Frizela
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.coverageNew York
dc.date.accessioned2020-07-02T18:52:09Z
dc.date.available2020-07-02T18:52:09Z
dc.date.issued2018
dc.description.abstractIn the heart, catecholamine effects occur by activation of beta-adrenergic receptors (beta-ARs), mainly the beta 1 (beta(1)-AR) and beta 2 (beta(2)-AR) subtypes, both of which couple to the Gs protein that activates the adenylyl cyclase signaling pathway. The beta(2)-ARs can also couple to the Gi protein that counterbalances the effect of the Gs protein on cyclic adenosine monophosphate production and activates the phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway. In several cardiovascular disorders, including heart failure, as well as in aging and in animal models of environmental stress, a reduction in the beta(1)/beta(2)-AR ratio and activation of the beta(2)-AR-Gi-PI3K-Akt signaling pathway have been observed. Recent studies have shown that sirtuins modulate certain organic processes, including the cellular stress response, through activation of the PI3K-Akt signaling pathway and of downstream molecules such as p53, Akt, HIF1-alpha, and nuclear factor-kappa B. In the heart, SIRT1, SIRT3, and beta(2)-ARs are crucial to the regulation of the cardiomyocyte energy metabolism, oxidative stress, reactive oxygen species production, and autophagy. SIRT1 and the beta(2)-AR-Gi complex also control signaling pathways of cell survival and death. Here, we review the role played by beta(2)-ARs and sirtuins during aging, heart failure, and adaptation to stress, focusing on the putative interplay between the two. That relationship, if proven, merits further investigation in the context of cardiac function and dysfunction.en
dc.description.affiliationUniv Fed Sao Paulo UNIFESP, Lab Stress Biol, Dept Biosci, Campus Baixada Santista, Santos, Brazil
dc.description.affiliationUniv Coimbra, Ctr Neurosci & Cell Biol CNC, Coimbra, Portugal
dc.description.affiliationUniv Coimbra, Sch Pharm, Coimbra, Portugal
dc.description.affiliationUniv Fed Espirito Santo, Dept Physiol Sci, HUCAM, Vitoria, Brazil
dc.description.affiliationUniv Fed Espirito Santo, Univ Hosp Cassiano Antonio de Moraes, HUCAM, Vitoria, Brazil
dc.description.affiliationUNIFESP, Dept Biociencias, Campus Baixada Santista,Rua Silva Jardim 136, BR-11015020 Santos, SP, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo UNIFESP, Lab Stress Biol, Dept Biosci, Campus Baixada Santista, Santos, Brazil
dc.description.affiliationUnifespUNIFESP, Dept Biociencias, Campus Baixada Santista,Rua Silva Jardim 136, BR-11015020 Santos, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt
dc.description.sponsorshipFundação de Amparo à Pesquisa do Espírito Santo (FAPES)pt
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt
dc.description.sponsorshipIDFAPESP: 2012/21990-6pt
dc.description.sponsorshipIDFAPES: 74087886pt
dc.description.sponsorshipIDCNPq: 424114/2016-0pt
dc.description.sponsorshipIDFAPESP: 2016/20777-8pt
dc.format.extent109-120
dc.identifierhttps://dx.doi.org/10.1007/s10571-017-0557-2
dc.identifier.citationCellular And Molecular Neurobiology. New York, v. 38, n. 1, p. 109-120, 2018.
dc.identifier.doi10.1007/s10571-017-0557-2
dc.identifier.issn0272-4340
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/53903
dc.identifier.wosWOS:000423033800010
dc.language.isoeng
dc.publisherSpringer/Plenum Publishers
dc.relation.ispartofCellular And Molecular Neurobiology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectEnvironmental stressen
dc.subjectAgingen
dc.subjectHeart failureen
dc.subjectAdrenergic receptorsen
dc.subjectSirtuinsen
dc.titleRole of beta-adrenergic receptors and sirtuin signaling in the heart during aging, heart failure, and adaptation to stressen
dc.typeinfo:eu-repo/semantics/article
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