Evidence map›Paper›PMID 39804990›Full record

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

TIA1-Mediated Stress Granules Promote the Neuroinflammation and Demyelination in Experimental Autoimmune Encephalomyelitis through Upregulating IL-31RA Signaling.

Xin Hua, Lingting Jin, Zheyu Fang, Yiyun Weng, Yuan Zhang, Jingjing Zhang, Dewei Xie, Yang Tang, Siyu Guo, Yingying Huang and 4 more

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Activation of Kir4.1 Channels by 2-D08 Promotes Myelin Repair in Multiple Sclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  11. Review
  12. Review
  13. 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

14 authors.

Xin HuaDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Lingting JinSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Zheyu FangDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Yiyun WengDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Yuan ZhangDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Jingjing ZhangSchool of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Dewei XieDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Yang TangCancer Institute, Second Affiliated Hospital, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, 310058, China.
Siyu GuoCancer Institute, Second Affiliated Hospital, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, 310058, China.
Yingying HuangDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Yilin DaiDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Jia LiDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Zhihui HuangDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Xu ZhangDepartment of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.ORCID https://orcid.org/0000-0002-3680-513X

Funding

National Natural Science Foundation of China 81971142
6 · The paper itself

Abstract

The dysfunction of stress granules (SGs) plays a crucial role in the pathogenesis of various neurological disorders, with T cell intracellular antigen 1 (TIA1) being a key component of SGs. However, the role and mechanism of TIA1-mediated SGs in experimental autoimmune encephalomyelitis (EAE) remain unclear. In this study, upregulation of TIA1, its translocation from the nucleus to the cytoplasm, and co-localization with G3BP1 (a marker of SGs) are observed in the spinal cord neurons of EAE mice. Deletion of TIA1 in the CNS alleviates neuroinflammation, suppresses demyelination and axonal damage, and reduces neuronal loss in EAE mice. Furthermore, alleviation of autophagy dysfunction and reduction of chronic persistent SGs are observed in Tia1

Indexed as

Demyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalNeuroinflammatory DiseasesStress GranulesT-Cell Intracellular Antigen-1AnimalsAutophagyFemaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionUp-RegulationT-Cell Intracellular Antigen-1Tia1 protein, mouseexperimental autoimmune encephalomyelitismultiple sclerosisneuroinflammationstress granulesT‐cell intracellular antigen 1

Identifiers

PMID39804990
PMCPMC11984900

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.