Regulation of SIRT1 and Its Roles in Inflammation

The silent information regulator sirtuin 1 (SIRT1) protein, a highly conserved NAD + -dependent deacetylase belonging to the sirtuin family, is a post-translational regulator that plays a role in modulating inflammation. SIRT1 affects multiple biological processes by deacetylating a variety of prote...

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Veröffentlicht in:Frontiers in immunology Jg. 13; S. 831168
Hauptverfasser: Yang, Yunshu, Liu, Yang, Wang, Yunwei, Chao, Yongyi, Zhang, Jinxin, Jia, Yanhui, Tie, Jun, Hu, Dahai
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland Frontiers Media S.A 11.03.2022
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ISSN:1664-3224, 1664-3224
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Zusammenfassung:The silent information regulator sirtuin 1 (SIRT1) protein, a highly conserved NAD + -dependent deacetylase belonging to the sirtuin family, is a post-translational regulator that plays a role in modulating inflammation. SIRT1 affects multiple biological processes by deacetylating a variety of proteins including histones and non-histone proteins. Recent studies have revealed intimate links between SIRT1 and inflammation, while alterations to SIRT1 expression and activity have been linked to inflammatory diseases. In this review, we summarize the mechanisms that regulate SIRT1 expression, including upstream activators and suppressors that operate on the transcriptional and post-transcriptional levels. We also summarize factors that influence SIRT1 activity including the NAD + /NADH ratio, SIRT1 binding partners, and post-translational modifications. Furthermore, we underscore the role of SIRT1 in the development of inflammation by commenting on the proteins that are targeted for deacetylation by SIRT1. Finally, we highlight the potential for SIRT1-based therapeutics for inflammatory diseases.
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Edited by: Bisheng Zhou, University of Illinois at Chicago, United States
Reviewed by: Haiying Wang, Peking University, China; Jiaxiang Chen, Mayo Clinic, United States
This article was submitted to Inflammation, a section of the journal Frontiers in Immunology
These authors have contributed equally to this work and share first authorship
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2022.831168