Use este identificador para citar ou linkar para este item: http://hdl.handle.net/1843/44561
Tipo: Artigo de Periódico
Título: Nuclear sirtuins and inflammatory signaling pathways
Autor(es): Keila Lopes Mendes
Deborah de Farias Lelis
Sérgio Henrique Sousa Santos
Resumo: The 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.
Assunto: Inflamação
Doenças crônicas
Síndrome metabólica
Obesidade
Diabetes
Artrite
Histonas
Idioma: eng
País: Brasil
Editor: Universidade Federal de Minas Gerais
Sigla da Instituição: UFMG
Departamento: ICA - INSTITUTO DE CIÊNCIAS AGRÁRIAS
Tipo de Acesso: Acesso Restrito
Identificador DOI: https://doi.org/10.1016/j.cytogfr.2017.11.001
URI: http://hdl.handle.net/1843/44561
Data do documento: Dez-2017
metadata.dc.url.externa: https://www.sciencedirect.com/science/article/pii/S1359610117301740?via%3Dihub
metadata.dc.relation.ispartof: Cytokine and Growth Factor Reviews
Aparece nas coleções:Artigo de Periódico

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