Evidence map›Paper›PMID 37622049›Full record

ReviewFrontiers in cellular neuroscience2023

New insights into Sirt1: potential therapeutic targets for the treatment of cerebral ischemic stroke.

Hao Tang, Jun Wen, Ting Qin, Yue Chen, Jiagui Huang, Qinghuan Yang, Peiran Jiang, Ling Wang, Yong Zhao, Qin Yang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

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  14. SIRT1 and miR-34a as Potential Plasma Biomarkers in the Acute Phase of Ischemic Stroke.International journal of molecular and cellular medicine · 2025
    Article
  15. Review
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  17. International journal of molecular sciences · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Hao Tang *Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jun Wen *Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ting Qin *Department of Respiratory Disease, Daping Hospital, Army Medical University, Chongqing, China.
Yue ChenDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jiagui HuangDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qinghuan YangDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Peiran JiangDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ling WangDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yong ZhaoDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qin YangDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is one of the main causes of mortality and disability worldwide. However, the majority of patients are currently unable to benefit from intravenous thrombolysis or intravascular mechanical thrombectomy due to the limited treatment windows and serious complications. Silent mating type information regulation 2 homolog 1 (Sirt1), a nicotine adenine dinucleotide-dependent enzyme, has emerged as a potential therapeutic target for ischemic stroke due to its ability to maintain brain homeostasis and possess neuroprotective properties in a variety of pathological conditions for the central nervous system. Animal and clinical studies have shown that activation of Sirt1 can lessen neurological deficits and reduce the infarcted volume, offering promise for the treatment of ischemic stroke. In this review, we summarized the direct evidence and related mechanisms of Sirt1 providing neuroprotection against cerebral ischemic stroke. Firstly, we introduced the protein structure, catalytic mechanism and specific location of Sirt1 in the central nervous system. Secondly, we list the activators and inhibitors of Sirt1, which are primarily divided into three categories: natural, synthetic and physiological. Finally, we reviewed the neuroprotective effects of Sirt1 in ischemic stroke and discussed the specific mechanisms, including reducing neurological deficits by inhibiting various programmed cell death such as pyroptosis, necroptosis, ferroptosis, and cuproptosis in the acute phase, as well as enhancing neurological repair by promoting angiogenesis and neurogenesis in the later stage. Our review aims to contribute to a deeper understanding of the critical role of Sirt1 in cerebral ischemic stroke and to offer novel therapeutic strategies for this condition.

Indexed as

cerebral ischemic strokedeacetylationneuroprotectionprogrammed cell deathSirt1

Identifiers

PMID37622049
PMCPMC10445043
OpenAlexW4385705771

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.