Evidence map›Paper›PMID 39792918›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

MicroRNA-204-5p Deficiency within the vmPFC Region Contributes to Neuroinflammation and Behavioral Disorders via the JAK2/STAT3 Signaling Pathway in Rats.

Xiao Chen, Yeting Gan, Kaiqi Zhang, Yuhan Wu, Ye Li, Tian Lan, Xianghua Zhuang, Shihong Chen, Shuyan Yu

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

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  10. [ModifiedNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
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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

9 authors.

Xiao ChenKey Laboratory of Mental Disorders, The Second Hospital of Shandong University, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Yeting GanKey Laboratory of Mental Disorders, The Second Hospital of Shandong University, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Kaiqi ZhangKey Laboratory of Mental Disorders, The Second Hospital of Shandong University, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Yuhan WuKey Laboratory of Mental Disorders, The Second Hospital of Shandong University, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Ye LiKey Laboratory of Mental Disorders, The Second Hospital of Shandong University, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Tian LanKey Laboratory of Mental Disorders, The Second Hospital of Shandong University, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Xianghua ZhuangDepartment of Endocrinology and Metabolism, The Second Hospital of Shandong University, Jinan, Shandong, 250033, China.
Shihong ChenDepartment of Endocrinology and Metabolism, The Second Hospital of Shandong University, Jinan, Shandong, 250033, China.
Shuyan YuKey Laboratory of Mental Disorders, The Second Hospital of Shandong University, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.ORCID https://orcid.org/0000-0001-6279-1088

Funding

National Natural Science Foundation of China NSFC 82070847National Natural Science Foundation of China NSFC 82071513
6 · The paper itself

Abstract

Major depressive disorder (MDD) is usually considered associate with immune inflammation and synaptic injury within specific brain regions. However, the molecular mechanisms underlying the neural deterioration resulting in depression remain unclear. Here, it is found that miR-204-5p is markedly downregulated in the ventromedial prefrontal cortex (vmPFC) in a chronic unpredictable mild stress (CUMS) induce rat model of depression. Knockdown of miR-204-5p in the vmPFC of normal rats results in depression and anxiety-like behaviors accompanied with the activation of microglia, elevated levels of pro-inflammatory cytokines, and increased numbers of neural apoptotic cells, effects which appear to be mediated by activation of the JAK2/STAT3 signaling pathway. Electrophysiological recordings further demonstrate that knockdown of miR-204-5p induces abnormal excitability of pyramidal neurons. In contrast, upregulation of miR-204-5p in the vmPFC of CUMS rats significantly causes inhibition of JAK2/STAT3 signaling pathway, improvements in neuronal impairments, and an abolition of the depression and anxiety-like behaviors. Moreover, pharmacological blocking of the JAK2/STAT3 signaling pathway significantly ameliorates abnormal behaviors resulting from miR-204-5p deficiency within the vmPFC. Collectively, these results provide robust evidence that the miR-204-5p/JAK2/STAT3 pathway may critically involve in the pathogenesis of depression, which may serve as potentially critical therapeutic target in the treatment of MDD.

Indexed as

Janus Kinase 2Major Depressive DisorderMicroRNAsNeuroinflammatory DiseasesPrefrontal CortexSTAT3 Transcription FactorAnimalsAnxietyBehavior, AnimalDepressionDisease Models, AnimalMaleRatsRats, Sprague-DawleySignal TransductionStress, PsychologicalJak2 protein, ratJanus Kinase 2MicroRNAsMIRN204 microRNA, ratStat3 protein, ratSTAT3 Transcription FactorJAK2/STAT3 signaling pathwayMDDmiR‐204‐5pneuroinflammationneuronal apoptosissynaptic plasticity

Identifiers

PMID39792918
PMCPMC11905084

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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.