Startseite The protective effects of activating Sirt1/NF-κB pathway for neurological disorders
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The protective effects of activating Sirt1/NF-κB pathway for neurological disorders

  • Yanhong Song , Ziyi Wu und Ping Zhao EMAIL logo
Veröffentlicht/Copyright: 8. November 2021
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Abstract

Sirt1, a member of the sirtuins family, is a nicotinamide adenosine dinucleotide (NAD+)-dependent deacetylase. It can be involved in the regulation of several processes including inflammatory response, apoptosis, oxidative stress, energy metabolism, and autophagy by exerting deacetylation. Nuclear factor-κB (NF-κB), a crucial nuclear transcription factor with specific DNA binding sequences, exists in almost all cells and plays a vital role in several biological processes involving inflammatory response, immune response, and apoptosis. As the hub of multiple intracellular signaling pathways, the activity of NF-κB is regulated by multiple factors. Sirt1 can both directly deacetylate NF-κB and indirectly through other molecules to inhibit its activity. We would like to emphasize that Sirt1/NF-κB is a signaling pathway that is closely related to neuroinflammation. Many recent studies have demonstrated the neuroprotective effects of Sirt1/NF-κB signaling pathway activation applied to the treatment of neurological related diseases. In this review, we focus on new advances in the neuroprotective effects of the Sirt1/NF-κB pathway. First, we briefly review Sirt1 and NF-κB, two key molecules of cellular metabolism. Next, we discuss the connection between NF-κB and neuroinflammation. In addition, we explore how Sirt1 regulates NF-κB in nerve cells and relevant evidence. Finally, we analyze the therapeutic effects of the Sirt1/NF-κB pathway in several common neuroinflammation-related diseases.


Corresponding author: Ping Zhao, Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang 110004, China, E-mail:

Funding source: National Nature Science Foundation of China

Award Identifier / Grant number: No. 82071215 to Ping Zhao; No. 82001154 to Ziyi Wu

Funding source: Outstanding Scientific Fund of Shengjing Hospital

Award Identifier / Grant number: No. 201708

  1. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  2. Research funding: This work was supported by the National Nature Science Foundation of China (No. 82071215 to Ping Zhao; No. 82001154 to Ziyi Wu) and the Outstanding Scientific Fund of Shengjing Hospital (No. 201708).

  3. Conflict of interest statement: The authors declare that there is no conflict of interest regarding the publication of this article.

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Received: 2021-09-05
Accepted: 2021-10-08
Published Online: 2021-11-08
Published in Print: 2022-06-27

© 2021 Walter de Gruyter GmbH, Berlin/Boston

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