Evidence map›Paper›PMID 34787377›Full record

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

Dysmyelination by Oligodendrocyte-Specific Ablation of Ninj2 Contributes to Depressive-Like Behaviors.

Yuxia Sun, Xiang Chen, Zhimin Ou, Yue Wang, Wenjing Chen, Tongjin Zhao, Changqin Liu, Ying Chen

Open access · goldAbstract 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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Ninjurin2 Promotes Pulmonary Endothelial Barrier Dysfunction Through VEGF/VEGFR2 Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  16. Necroptosis in CNS diseases: Focus on astrocytes.Frontiers in aging neuroscience · 2022
    Review
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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

8 authors at 3 institutions in 1 country.

Yuxia SunState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361005, China.
Xiang ChenState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361005, China.
Zhimin OuState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361005, China.
Yue WangState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361005, China.
Wenjing ChenState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361005, China.
Tongjin ZhaoShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Changqin LiuDepartment of Endocrinology and Diabetes, The First Affiliated Hospital of Xiamen University, Fujian Province Key Laboratory of Diabetes Translational Medicine, Xiamen, Fujian, 361101, China.
Ying ChenState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361005, China.ORCID 0000-0001-5675-1928
Xiamen University · CNFirst Affiliated Hospital of Xiamen University · CNSun Yat-sen University · CN

Funding

National Natural Science Foundation of China 31771122National Natural Science Foundation of China 32070966National Natural Science Foundation of China 81870611
6 · The paper itself

Abstract

Depression is a mental disorder affecting more than 300 million people in the world. Abnormalities in white matter are associated with the development of depression. Here, the authors show that mice with oligodendrocyte-specific deletion of Nerve injury-induced protein 2 (Ninj2) exhibit depressive-like behaviors. Loss of Ninj2 in oligodendrocytes inhibits oligodendrocyte development and myelination, and impairs neuronal structure and activities. Ninj2 competitively inhibits TNFα/TNFR1 signaling pathway by directly binding to TNFR1 in oligodendrocytes. Loss of Ninj2 activates TNFα-induced necroptosis, and increases C-C Motif Chemokine Ligand 2 (Ccl2) production, which might mediate the signal transduction from oligodendrocyte to neurons. Inhibition of necroptosis by Nec-1s administration synchronously restores oligodendrocyte development, improves neuronal excitability, and alleviates depressive-like behaviors. This study thus illustrates the role of Ninj2 in the development of depression and myelination, reveals the relationship between oligodendrocytes and neurons, and provides a potential therapeutic target for depression.

Indexed as

AnimalsCell Adhesion Molecules, NeuronalDemyelinating DiseasesDepressive DisorderDisease Models, AnimalMiceMice, KnockoutOligodendrogliaRatsRats, Sprague-DawleySignal TransductionCell Adhesion Molecules, NeuronalNinj2 protein, mousedepressionnecroptosisNinj2oligodendrocytes

Identifiers

PMID34787377
PMCPMC8787401
OpenAlexW3213122472

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.