Evidence map›Paper›PMID 41053809›Full record

ArticleCell & bioscience2025

HnRNP M expression rescues neurodegeneration in neuronal intranuclear inclusion disease mouse model by restoring dysregulated RNA splicing and transcription.

Yongcheng Pan, Yangping Li, Ying Jiang, Xinhui Wang, Juan Wan, Qiying Sun, Yun Tian, Lu Shen, Hong Jiang, Beisha Tang and 2 more

Abstract read
In one paragraph

Article in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Yongcheng Pan *Department of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.ORCID http://orcid.org/0000-0001-5317-3675
Yangping Li *Department of Human Genetics, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Ying JiangCentre for Medical Genetics and Hunan Key Laboratory of Medical Genetics, School of Life Sciences, Central South University, Changsha, 410078, Hunan, China.
Xinhui WangDepartment of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Juan WanDepartment of Neurology, Multi-Omics Research Center for Brain Disorders, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421000, Hunan, China.
Qiying SunDepartment of Geriatrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yun TianDepartment of Geriatrics, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Lu ShenDepartment of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Hong JiangDepartment of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Beisha TangDepartment of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Bing YaoDepartment of Human Genetics, Emory University School of Medicine, Atlanta, GA, 30322, USA. bing.yao@emory.edu.
Qiong LiuDepartment of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. lqiong66@csu.edu.cn.ORCID http://orcid.org/0000-0002-2591-8550

Funding

National Natural Science Foundation of China 32071037National Natural Science Foundation of China 82171256National Natural Science Foundation of China 82171843National Natural Science Foundation of China 82394420National Natural Science Foundation of China 82394421National Natural Science Foundation of China U20A20355Natural Science Foundation of Hunan Province 2023JJ10097Natural Science Foundation of Hunan Province 2025JJ20079
6 · The paper itself

Abstract

backgroundNeuronal intranuclear inclusion disease (NIID) is a neurodegenerative disease caused by the expanded GGC repeats in the NOTCH2NLC gene, yet its underlying pathogenic mechanisms remains to be fully elucidated. Previous study suggests that hnRNP M, an RNA-binding protein sequestered into the inclusions, may contribute to RNA processing defects in NIID.

resultsIn this study, we investigated the role of hnRNP M in NIID pathogenesis by utilizing a NOTCH2NLC-98GGC transgenic mouse model that faithfully recapitulates key NIID phenotypes. We found that AAV-mediated hnRNP M expression partially alleviated neuropathological features, such as neuronal loss and gliosis, and improved motor deficits in NIID mice. Transcriptome analysis further revealed that hnRNP M expression restored transcriptional and splicing dysregulation in synapse- and neurodegeneration-related genes, such as Dlg and Smn.

conclusionsOur study established hnRNP M as a key regulator of NIID pathogenesis by modulating RNA transcription and splicing, underscoring the potential of targeting RNA processing abnormalities as a therapeutic strategy.

Indexed as

HnRNP MNeurodegenerationNIIDRNA splicingRNA transcription

Identifiers

PMID41053809
PMCPMC12502245

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.