Evidence map›Paper›PMID 42115187›Full record

ArticleTranslational psychiatry2026

Gut microbiota dysbiosis drives depression-like behavior in adolescent rats via lysine-regulated mTOR autophagy pathway.

Jushuang Zhang, Fei Chen, Xiaoxia Xu, Lige Zhang, Luman Zhang, Bingjie Qin, Kunyao Li, Quanbing Liu, Hanchen Hou, Yao Li and 6 more

Abstract read
In one paragraph

Article in Translational psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Jushuang Zhang *Department of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Fei Chen *Department of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Xiaoxia XuDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Lige ZhangDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Luman ZhangDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Bingjie QinDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Kunyao LiDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Quanbing LiuDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Hanchen HouDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yao LiDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Chenxi LiuDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Yinan LiDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Jiaqi ShiDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Teng TengDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. tengteng@hospital.cqmu.edu.cn.
Chao WangDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. Chwa0028@live.com.
Xinyu ZhouDepartment of Psychiatry, Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. zhouxinyu@cqmu.edu.cn.ORCID http://orcid.org/0000-0003-1908-0357

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The prevalence of major depressive disorder (MDD) is increasing globally, particularly among adolescents. Although gut-brain axis dysfunction has been implicated in adolescent depression, the mechanisms by which gut microbiota dysbiosis drives depressive behaviors and potential antidepressant targets remain unclear. In this study, fecal microbiota transplantation (FMT) was performed from either healthy controls (HCs) or adolescents with MDD into antibiotic-treated adolescent rats. FMT from MDD adolescents induced depressive-like behaviors in recipient rats. Metagenomic sequencing revealed that FMT from MDD adolescents led to alterations in gut microbiota in recipient rats. While qPCR, Western blotting, immunofluorescence, and transmission electron microscopy (TEM) confirmed that these rats exhibited prefrontal cortex (PFC) autophagy hyperactivation, evidenced by a reduction in SQSTM1/p62 levels, an elevation in the LC3-II/LC3-I ratio, upregulated Beclin1, and increased numbers of autolysosomes. Similar autophagy-related transcriptional changes were observed in peripheral blood from MDD adolescents. Furthermore, ELISA showed reduced plasma lysine levels in MDD adolescents and decreased lysine concentrations in the PFC of FMT-MDD rats. The antidepressant effect of lysine and its interaction with autophagy were explored in a chronic unpredictable mild stress (CUMS) rat model with or without rapamycin (the autophagy activator, RAPA). Lysine supplementation alleviated depressive-like behaviors and suppressed PFC autophagy hyperactivation, while these effects were abolished by RAPA co-treatment. These findings reveal lysine deficiency as a metabolic bridge between gut microbiota imbalance and neuronal autophagy dysregulation, suggesting a gut microbiota-lysine-autophagy axis as an innovative mechanism and therapeutic focus for adolescent depression.

Indexed as

AutophagyDysbiosisGastrointestinal MicrobiomeLysineMajor Depressive DisorderTOR Serine-Threonine KinasesAdolescentAnimalsBehavior, AnimalDepressionDisease Models, AnimalFecal Microbiota TransplantationHumansMalePrefrontal CortexRatsLysinemTOR protein, ratSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID42115187
PMCPMC13328664

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.