Regulatory Roles for SIRT1 in Aging and Immunosenescence
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Citation of Original Publication
Brissett-Lasalle, Devonique, Zoya Syed, Yashitha Yarubandi, Jeff Leips, and Erin Green. “Regulatory Roles for SIRT1 in Aging and Immunosenescence.” In Histone and Non-Histone Reversible Acetylation in Development, Aging and Disease, edited by Marta Halasa and Anna Wawruszak. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-91459-1_10.
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This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: http://dx.doi.org/doi.org/10.1007/978-3-031-91459-1_10
Abstract
Silent information regulator 1 (SIRT1), a conserved lysine deacetylase, is an important contributor to the function of macrophages, which are the scavengers of the innate immune system. Macrophages are part of the first line of defense against infection and key players in immunity due to their ability to survey tissue for infections or damage, release inflammatory cytokines, and clear pathogens. Macrophage function deteriorates with age and is a common indicator of immunosenescence. SIRT1 is known to influence multiple aspects of macrophage physiology, particularly proliferation, self-renewal, migration, the regulation of macrophage polarization, and the ability of macrophages to clear pathogens via phagocytosis and inflammasome signaling. Furthermore, mammalian SIRT1 and orthologous Sir2 in other organisms have well-defined roles in aging. Therefore, in this chapter, we discuss evidence that links SIRT1 to macrophage behavior and function, explore its role in inflammatory pathways linked to aging, and highlight key research questions in immunosenescence and the implications for epigenetic and non-epigenetic roles of SIRT1.