Evidence map›Paper›PMID 37013604›Full record

ArticleActa neuropathologica communications2023

Upregulation of carbonic anhydrase 1 beneficial for depressive disorder.

Ke Cheng, Yue Wang, Yong He, Yu Tian, Junjie Li, Chong Chen, Xingzhe Xu, Zhonghao Wu, Heming Yu, Xiangyu Chen and 5 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

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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

15 authors at 5 institutions in 1 country.

Ke Cheng *NHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yue Wang *NHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yong He *NHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yu Tian *NHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Junjie Li *Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Chongqing, 400014, China.
Chong ChenNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xingzhe XuNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Zhonghao WuNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Heming YuDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xiangyu ChenDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yili WuOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Zhejiang Provincial Clinical Research Center for Mental Disorders, Key Laboratory of Alzheimer's Disease of Zhejiang Province, School of Mental Health and Kangning Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Weihong SongOujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), Institute of Aging, Zhejiang Provincial Clinical Research Center for Mental Disorders, Key Laboratory of Alzheimer's Disease of Zhejiang Province, School of Mental Health and Kangning Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China. weihong@mail.ubc.ca.ORCID 0000-0001-9928-889X
Zhifang DongMinistry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Chongqing, 400014, China. zfdong@cqmu.edu.cn.
Huatai XuInstitute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China. xuhuatai@ion.ac.cn.
Peng XieNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. xiepeng58@21cn.com.
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNChinese Academy of Sciences · CNWenzhou Medical University · CNChildren's Hospital of Chongqing Medical University · CNChina International Science and Technology Cooperation · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carbonic Anhydrase 1 (CAR1) is a zinc-metalloenzyme that catalyzes the hydration of carbon dioxide, and the alteration of CAR1 has been implicated in neuropsychiatric disorders. However, the mechanism underlying the role of CAR1 in major depressive disorder (MDD) remains largely unknown. In this study, we report the decreased level of CAR1 in MDD patients and depression-like model rodents. We found that CAR1 is expressed in hippocampal astrocytes and CAR1 regulates extracellular bicarbonate concentration and pH value in the partial hilus. Ablation of the CAR1 gene increased the activity of granule cells via decreasing their miniature inhibitory postsynaptic currents (mIPSC), and caused depression-like behaviors in CAR1-knockout mice. Astrocytic CAR1 expression rescued the deficits in mIPSCs of granule cells and reduced depression-like behaviors in CAR1 deficient mice. Furthermore, pharmacological activation of CAR1 and overexpression of CAR1 in the ventral hippocampus of mice improved depressive behaviors. These findings uncover a critical role of CAR1 in the MDD pathogenesis and its therapeutic potential.

Indexed as

Carbonic AnhydrasesMajor Depressive DisorderAnimalsMiceMice, KnockoutTranscriptional ActivationUp-RegulationCarbonic AnhydrasesCAR1-knockout miceCarbonic anhydrase 1Hippocampal astrocytesMajor depressive disorderMiniature inhibitory postsynaptic currents

Identifiers

PMID37013604
PMCPMC10071615
OpenAlexW4362523032

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.