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REVIEW article
Front. Pharmacol.
Sec. Neuropharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1425560
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Ischemic stroke, the most prevalent form of stroke, is responsible for the highest disability rates globally and ranks as the primary cause of mortality worldwide. Sirt1, extensively investigated in neurodegenerative disorders, is the most well-known and earliest member of the sirtuins family.However, its mechanism of action during ischemic stroke remains ambiguous. The literature examination revealed the intricate involvement of Sirt1 in regulating both physiological and pathological mechanisms during ischemic stroke. Sirt1 demonstrates deacetylation effects on PGC-1 α, HMGB1, FOXOs, and p53. It hinders the activation of NLRP3 inflammasome and NF-κB while also engaging with AMPK. It regulates inflammatory response, oxidative stress, mitochondrial dysfunction, autophagy, pro-death, and necrotic apoptosis. Therefore, the potential of Sirt1 as a therapeutic target for the management of ischemic stroke is promising.
Keywords: ischemic stroke, SIRT1, Inflammation, Oxidative Stress, Autophagy, Mitochondrial dysfunction, Pan-apoptosis
Received: 30 Apr 2024; Accepted: 25 Feb 2025.
Copyright: © 2025 Jia, Xu, Li, Yang, Chen, Zhang, Li and Sun. 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) or licensor 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.
* Correspondence:
Shulin Li, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang Province, China
XiaoWei Sun, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang Province, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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