Evidence map›Paper›PMID 40470772›Full record

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

Activation of Kir4.1 Channels by 2-D08 Promotes Myelin Repair in Multiple Sclerosis.

Mingdong Liu, Shengyu Jin, Xin Fu, Chong Xie, Yi Chen, Liangtang Chang, Yongheng Fan, Donghua He, Xiaoqi Hong, Xi Shen and 8 more

Abstract read
PubMed Full text at PMC Publisher
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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Activation of Kir4.1 Channels by 2-D08 Promotes Myelin Repair in Multiple Sclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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

18 authors.

Mingdong LiuDepartment of Obstetrics and Gynecology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.
Shengyu JinDepartment of Obstetrics and Gynecology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.
Xin FuCenter for Brain Science, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Chong XieDepartment of Neurology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Yi ChenDepartment of Neurology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Liangtang ChangInstitute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China.
Yongheng FanInstitute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China.
Donghua HeInstitute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China.
Xiaoqi HongDepartment of Obstetrics and Gynecology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.
Xi ShenDepartment of Obstetrics and Gynecology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.
Xiaoli ZhengDepartment of Obstetrics and Gynecology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.
Qiyue WangFrontiers Science Center for Transformative Molecules, School of Chemistry and Chemical Engineering, School of Biomedical Engineering, National Center for Translational Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Dao ShiFrontiers Science Center for Transformative Molecules, School of Chemistry and Chemical Engineering, School of Biomedical Engineering, National Center for Translational Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Fangyuan LiSongjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.
Daishun LingFrontiers Science Center for Transformative Molecules, School of Chemistry and Chemical Engineering, School of Biomedical Engineering, National Center for Translational Medicine, Shanghai Jiao Tong University, Shanghai, 200240, China.
Yangtai GuanDepartment of Neurology, Punan Branch of Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200125, China.ORCID https://orcid.org/0000-0003-0813-4073
Neng GongInstitute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China.
Xiaoping TongDepartment of Obstetrics and Gynecology, Songjiang Research Institute, Shanghai Key Laboratory of Emotions and Affective Disorders, Songjiang Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 201600, China.ORCID https://orcid.org/0000-0002-0908-8091

Funding

Innovative Research Team of High-level Local Universities SHSMU-ZDCX20211901National Natural Science Foundation of China 31571063National Natural Science Foundation of China 31970904National Natural Science Foundation of China 82271466National Natural Science Foundation of China 91632104Shanghai Municipal Science and Technology Major Project 2018SHZDZX05the STI2030-Major Projects 2022ZD0204700
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease that leads to myelin loss and neurological dysfunction. Clinical studies show increased anti-Kir4.1 antibody levels in MS patients' serum, indicating its diagnostic potential. However, the specific mechanism has remained elusive. In a mouse model of experimental autoimmune encephalomyelitis (EAE), it is found that impaired Kir4.1 channels in oligodendrocyte precursor cells (OPCs) hindered myelin repair in the spinal cord. Using a thermal shift assay (TSA), the small molecule 2-D08 is identified, which effectively activated Kir4.1 channels and reduced demyelination in both EAE mice and marmosets. The neuroprotective effects are mainly due to enhanced phosphorylation of FYN tyrosine kinase, promoting OPCs differentiation. The findings highlight the critical role of Kir4.1 channels in MS pathogenesis and suggest that pharmacological activation of these channels by 2-D08 can be a promising therapeutic strategy for enhancing brain recovery in demyelinating diseases.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisMyelin SheathPotassium Channels, Inwardly RectifyingAnimalsDisease Models, AnimalFemaleHumansKcnj10 ChannelMiceMice, Inbred C57BLOligodendrocyte Precursor CellsOligodendrogliaKcnj10 ChannelPotassium Channels, Inwardly Rectifying2‐D08demyelinating diseasesKir4.1multiple sclerosisremyelination

Identifiers

PMID40470772
PMCPMC12442624

What Socratic 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 Socratic graph.