Evidence map›Paper›PMID 36414403›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022

Genetic and Pharmacological Inhibition of Astrocytic Mysm1 Alleviates Depressive-Like Disorders by Promoting ATP Production.

Heyang Zhang, Shuirong Liu, Qiaozhen Qin, Zhenhua Xu, Yannv Qu, Yadi Wang, Jianing Wang, Zhangzhen Du, Shanshan Yuan, Shunming Hong and 8 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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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

18 authors.

Heyang ZhangBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.ORCID https://orcid.org/0000-0002-6047-6874
Shuirong LiuBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Qiaozhen QinBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Zhenhua XuBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Yannv QuDepartment of Geriatrics, Peking University Shenzhen Hospital, Shenzhen, Guangzhou, 518036, China.
Yadi WangBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Jianing WangBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Zhangzhen DuBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Shanshan YuanBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Shunming HongBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Zhilin ChangChina National Clinical Research Center for Neurological Diseases, Jing-Jin Center for Neuroinflammation, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.
Wenyan HeChina National Clinical Research Center for Neurological Diseases, Jing-Jin Center for Neuroinflammation, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.
Xinlong YanFaculty of Environmental and Life Sciences, Beijing University of Technology, Beijing, 100124, China.
Yiran LangBeijing Innovation Center for Intelligent Robots and Systems, Beijing Institute of Technology, Beijing, 100081, China.
Rongyu TangBeijing Innovation Center for Intelligent Robots and Systems, Beijing Institute of Technology, Beijing, 100081, China.
Yan WangBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Lingling ZhuBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.
Xiaoxia JiangBeijing Institute of Basic Medical Sciences, 27 Taiping Road, Haidian District, Beijing, 100850, China.

Funding

Beijing Natural Science Foundation 7202149National Natural Science Foundation of China 31971285National Natural Science Foundation of China 82072104
6 · The paper itself

Abstract

Major depressive disorder (MDD) is a leading cause of disability worldwide. A comprehensive understanding of the molecular mechanisms of this disorder is critical for the therapy of MDD. In this study, it is observed that deubiquitinase Mysm1 is induced in the brain tissues from patients with major depression and from mice with depressive behaviors. The genetic silencing of astrocytic Mysm1 induced an antidepressant-like effect and alleviated the osteoporosis of depressive mice. Furthermore, it is found that Mysm1 knockdown led to increased ATP production and the activation of p53 and AMP-activated protein kinase (AMPK). Pifithrin α (PFT α) and Compound C, antagonists of p53 and AMPK, respectively, repressed ATP production and reversed the antidepressant effect of Mysm1 knockdown. Moreover, the pharmacological inhibition of astrocytic Mysm1 by aspirin relieved depressive-like behaviors in mice. The study reveals, for the first time, the important function of Mysm1 in the brain, highlighting astrocytic Mysm1 as a potential risk factor for depression and as a valuable target for drug discovery to treat depression.

Indexed as

antidepressant effectaspirinastrocyteATPMysm1

Identifiers

PMID36414403
PMCPMC9811473

What OpenQuestion holds

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Registered trials

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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.