Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/44561
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dc.creatorKeila Lopes Mendespt_BR
dc.creatorDeborah de Farias Lelispt_BR
dc.creatorSérgio Henrique Sousa Santospt_BR
dc.date.accessioned2022-08-25T13:40:55Z-
dc.date.available2022-08-25T13:40:55Z-
dc.date.issued2017-12-
dc.citation.volume38pt_BR
dc.citation.spage98pt_BR
dc.citation.epage105pt_BR
dc.identifier.doihttps://doi.org/10.1016/j.cytogfr.2017.11.001pt_BR
dc.identifier.issn1879-0305pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/44561-
dc.description.resumoThe regulation of chronic inflammation has received considerable research attention in recent years because of its contribution to the pathogenesis of chronic diseases such as arthritis, diabetes, metabolic syndrome and obesity. Thus, strategies that inhibit the inflammatory state may be beneficial in improving the pathophysiology of several inflammation-related disorders. Sirtuins are a family of histone deacetylases that contain seven enzymatic activities in mammals (SIRT1–SIRT7) and function to suppress gene transcription by epigenetic mechanisms. Nuclear sirtuins (SIRT 1, 2, 6 and 7) in particular may play an important role in the regulation of inflammatory responses. In the present review, we assessed the roles of nuclear sirtuins in inflammatory reactions: SIRT1 has been shown to suppress NF-κb activity, the master regulator of cellular inflammatory response, decrease COX-2 and iNOS production, and increase antioxidant gene expression that suppressed inflammation. SIRT2 activity included the deacetylation of p65 subunit of NF-κβ and RIP-1, while SIRT6 has been shown to interact with p65/RelA bound to the NF-κβ promoter region and repress transcriptional activity. Furthermore, recent studies have shown that the absence of SIRT7 produced an increase in inflammation, illustrating that SIRT7 also functioned to decrease inflammation. Given their significant roles in the regulation of chronic inflammation, nuclear sirtuins represent potential therapeutic targets in the control of chronic inflammatory diseases.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Geraispt_BR
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentICA - INSTITUTO DE CIÊNCIAS AGRÁRIASpt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofCytokine and Growth Factor Reviewspt_BR
dc.rightsAcesso Restritopt_BR
dc.subject.otherInflamaçãopt_BR
dc.subject.otherDoenças crônicaspt_BR
dc.subject.otherSíndrome metabólicapt_BR
dc.subject.otherObesidadept_BR
dc.subject.otherDiabetespt_BR
dc.subject.otherArtritept_BR
dc.subject.otherHistonaspt_BR
dc.titleNuclear sirtuins and inflammatory signaling pathwayspt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.sciencedirect.com/science/article/pii/S1359610117301740?via%3Dihubpt_BR
Appears in Collections:Artigo de Periódico

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