Evidence map›Paper›PMID 36357867›Full record

ArticleBMC neuroscience2022

Involvement of kynurenine pathway between inflammation and glutamate in the underlying etiopathology of CUMS-induced depression mouse model.

Xingying Wu, Bowen Chen, Zhong Di, Shuo Jiang, Haipeng Xu, Mengting Shi, Rong Hu, Shaopeng Sun, Zhujin Song, Jiapeng Liu and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
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  6. Metabolic Reprogramming of Microglia in Neuroinflammation and Depression.International journal of molecular sciences · 2026
    Review
  7. Article
  8. Antidepressant and Cognitive-Enhancing Effects ofPharmaceuticals (Basel, Switzerland) · 2026
    Article
  9. Review
  10. Article
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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

12 authors at 2 institutions in 1 country.

Xingying Wu *Department of Neurobiology and Acupuncture Research, The Third School of Clinical Medicine (School of Rehabilitation Medicine), Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, China.
Bowen Chen *Department of Neurobiology and Acupuncture Research, The Third School of Clinical Medicine (School of Rehabilitation Medicine), Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, China.
Zhong DiDepartment of Acupuncture and Moxibustion, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310000, People's Republic of China.
Shuo JiangDepartment of Acupuncture and Moxibustion, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310000, People's Republic of China.
Haipeng XuDepartment of Neurobiology and Acupuncture Research, The Third School of Clinical Medicine (School of Rehabilitation Medicine), Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, China.
Mengting ShiDepartment of Neurobiology and Acupuncture Research, The Third School of Clinical Medicine (School of Rehabilitation Medicine), Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, China.
Rong HuDepartment of Neurobiology and Acupuncture Research, The Third School of Clinical Medicine (School of Rehabilitation Medicine), Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, China.
Shaopeng SunThe First Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Zhujin SongBasic Medical College, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Jiapeng LiuDepartment of Neurobiology and Acupuncture Research, The Third School of Clinical Medicine (School of Rehabilitation Medicine), Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, China.
Ruijie MaDepartment of Neurobiology and Acupuncture Research, The Third School of Clinical Medicine (School of Rehabilitation Medicine), Key Laboratory of Acupuncture and Neurology of Zhejiang Province, Zhejiang Chinese Medical University, Hangzhou, China. maria7878@sina.com.
Qin GuoDepartment of Acupuncture and Moxibustion, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310000, People's Republic of China. 20165019@zcmu.edu.cn.
The Third Affiliated Hospital of Zhejiang Chinese Medical University · CNZhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation and glutamate (GLU) are widely thought to participate in the pathogenesis of depression, and current evidence suggests that the development of depression is associated with the activation of the kynurenine pathway (KP). However, the exact mechanism of KP among the inflammation, GLU and depression remain poorly understood. In this study, we examined the involvement of KP, inflammation and GLU in depressive phenotype induced by chronic unpredictable mild stress (CUMS) in C57B/6 J mice. Our results showed that CUMS caused depressive like-behavior in the sucrose preference test, tail suspension test and forced swimming test. From a molecular perspective, CUMS upregulated the peripheral and central inflammatory response and activated indoleamine 2,3-dioxygenase (IDO), the rate-limiting enzyme of KP, which converts tryptophan (TRP) into kynurenine (KYN). KYN is a precursor for QA in microglia, which could activate the N-methyl-D-aspartate receptor (NMDAR), increasing the GLU release, mirrored by increased IDO activity, quinolinic acid and GLU levels in the hippocampus, prefrontal cortex and serum. However, intervention with IDO inhibitor 1-methyl-DL-tryptophan (50 mg/kg/s.c.) and 1-methyl-L-tryptophan (15 mg/kg/i.p.) reversed the depressive-like behaviors and adjusted central and peripheral KP's metabolisms levels as well as GLU content, but the inflammation levels were not completely affected. These results provide certain evidence that KP may be a vital pathway mediated by IDO linking inflammation and glutamate, contributing to depression.

Indexed as

DepressionKynurenineAnimalsDisease Models, AnimalGlutamic AcidIndoleamine-Pyrrole 2,3,-DioxygenaseInflammationMiceTryptophanGlutamic AcidIndoleamine-Pyrrole 2,3,-DioxygenaseKynurenineTryptophanChronic unpredictable mild stressDepressionGlutamateInflammationKynurenine pathway

Identifiers

PMID36357867
PMCPMC9650798
OpenAlexW4309072789

What OpenQuestion holds

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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.