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      Regulation of SIRT1 and Its Roles in Inflammation


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          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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          Most cited references175

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          Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016.

          To provide an update to "Surviving Sepsis Campaign Guidelines for Management of Sepsis and Septic Shock: 2012".
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            Sepsis and septic shock

            Sepsis is a common condition that is associated with unacceptably high mortality and, for many of those who survive, long-term morbidity. Increased awareness of the condition resulting from ongoing campaigns and the evidence arising from research in the past 10 years have increased understanding of this problem among clinicians and lay people, and have led to improved outcomes. The World Health Assembly and WHO made sepsis a global health priority in 2017 and have adopted a resolution to improve the prevention, diagnosis, and management of sepsis. In 2016, a new definition of sepsis (Sepsis-3) was developed. Sepsis is now defined as infection with organ dysfunction. This definition codifies organ dysfunction using the Sequential Organ Failure Assessment score. Ongoing research aims to improve definition of patient populations to allow for individualised management strategies matched to a patient's molecular and biochemical profile. The search continues for improved diagnostic techniques that can facilitate this aim, and for a pharmacological agent that can improve outcomes by modifying the disease process. While waiting for this goal to be achieved, improved basic care driven by education and quality-improvement programmes offers the best hope of increasing favourable outcomes.
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              Shared principles in NF-kappaB signaling.

              The transcription factor NF-kappaB has served as a standard for inducible transcription factors for more than 20 years. The numerous stimuli that activate NF-kappaB, and the large number of genes regulated by NF-kappaB, ensure that this transcription factor is still the subject of intense research. Here, we attempt to synthesize some of the basic principles that have emerged from studies of NF-kappaB, and we aim to generate a more unified view of NF-kappaB regulation.

                Author and article information

                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                11 March 2022
                : 13
                [1] 1 Department of Burns and Cutaneous Surgery, Xijing Hospital, Fourth Military Medical University , Xi’an, China
                [2] 2 Department of Emergency, Xijing Hospital, Fourth Military Medical University , Xi’an, China
                [3] 3 State Key Laboratory of Cancer Biology and Xijing Hospital of Digestive Diseases, Xijing Hospital, Fourth Military Medical University , Xi’an, China
                Author notes

                Edited by: Bisheng Zhou, University of Illinois at Chicago, United States

                Reviewed by: Haiying Wang, Peking University, China; Jiaxiang Chen, Mayo Clinic, United States

                *Correspondence: Dahai Hu, hudhai@ 123456fmmu.edu.cn ; Jun Tie, tiejun7776@ 123456163.com

                †These authors have contributed equally to this work and share first authorship

                This article was submitted to Inflammation, a section of the journal Frontiers in Immunology

                Copyright © 2022 Yang, Liu, Wang, Chao, Zhang, Jia, Tie and Hu

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 4, Tables: 2, Equations: 0, References: 175, Pages: 16, Words: 7033
                Funded by: National Natural Science Foundation of China , doi 10.13039/501100001809;
                Award ID: 81530064, 81773071, 81972226
                Funded by: Natural Science Foundation of Shaanxi Province , doi 10.13039/501100007128;
                Award ID: 2021JM-249

                sirt1,gene regulation,enzyme activity,post-translational modification,inflammation
                sirt1, gene regulation, enzyme activity, post-translational modification, inflammation


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