Evidence mapPaperPMID 42503585Full record

ArticleMolecular neurobiology2026

Early Rehabilitation Exercise Promotes Vestibular Compensation in UVN Mice by Regulating Microglial Polarization Balance via the PGC-1α/FNDC5/BDNF Pathway.

Junyu Wu, Zhihui Zheng, Gengxin Lu, Junjie Guo, Minping Li, Dongxiao Zhou, Xiaoqiu Liang, Weiwei Qi, Xue Xu, Zhezhi Deng and 1 more

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

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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

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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

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4 · The record

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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

11 authors.

Junyu Wu *Department of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Zhihui Zheng *Department of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Gengxin LuDepartment of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Junjie GuoDepartment of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Minping LiDepartment of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Dongxiao ZhouDepartment of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Xiaoqiu LiangDepartment of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Weiwei QiDepartment of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Xue XuDepartment of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Zhezhi DengDepartment of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China. dengzhzh5@mail.sysu.edu.cn.
Haiwei HuangDepartment of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China. huanghw@mail.sysu.edu.cn.ORCID https://orcid.org/0000-0001-5663-8204

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2023A1515010491Basic and Applied Basic Research Foundation of Guangdong Province 2024A1515012456Guangdong Province International Cooperation Base for Early Intervention and Functional Rehabilitation of Neurological Diseases 2020A0505020004Guangdong Provincial Clinical Research Center for Neurological Diseases 2020B1111170002Guangzhou Basic and Applied Basic Research Foundation 2023A04J2199Guangzhou Basic and Applied Basic Research Foundation 2024A04J4565National Natural Science Foundation of China 82271410
6 · The paper itself

Abstract

Acute unilateral vestibular lesions cause disabling vertigo, postural imbalance, and gait instability. Functional recovery depends on vestibular compensation (VC), a neuroplastic process whose cellular and molecular mechanisms remain incompletely understood. Although vestibular rehabilitation effectively accelerates recovery in clinical practice, the underlying pathways are still elusive. Here, we investigated how exercise-based vestibular rehabilitation modulates neuroinflammation and microglial polarization within the medial vestibular nucleus (MVN) in a mouse model of unilateral vestibular neurectomy (UVN), focusing on the PGC‑1α/FNDC5/BDNF axis in promoting VC. Mice underwent a progressive running-wheel training protocol, and behavioural recovery was assessed using rotarod, beam-walk, and open-field tests. At the molecular and cellular levels, we combined mRNA sequencing, bioinformatic analysis, Western blotting, and immunofluorescence to evaluate pathway activation, inflammatory mediators, and microglial morphology and phenotype. Exercise upregulated the PGC‑1α/FNDC5/BDNF cascade and inhibited NF‑κB/NLRP3-mediated neuroinflammation. It also shifted microglia from a pro-inflammatory M1-like phenotype toward an anti-inflammatory M2-like state, increased microglial process complexity, and improved postural balance recovery. Intracerebroventricular administration of the PGC‑1α inhibitor SR‑18292 abrogated these effects, aggravating inflammation and delaying VC. These findings demonstrate that the PGC‑1α/FNDC5/BDNF pathway is a key mediator of exercise-promoted VC and a promising target for improving rehabilitation strategies for vestibular disorders.

Indexed as

Brain-Derived Neurotrophic FactorMicrogliaPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhysical Conditioning, AnimalSignal TransductionVestibule, LabyrinthAnimalsMaleMiceMice, Inbred C57BLBrain-Derived Neurotrophic FactorPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseMicrogliaNeuroinflammationPGC‑1α/FNDC5/BDNF axisUnilateral vestibular dysfunctionVestibular rehabilitation

Identifiers

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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.