Evidence map›Paper›PMID 29577640›Full record

ArticleCNS neuroscience & therapeutics2018

A Kv1.3 channel-specific blocker alleviates neurological impairment through inhibiting T-cell activation in experimental autoimmune encephalomyelitis.

Xiao-Lu Yuan, Yi-Peng Zhao, Jie Huang, Jun-Chen Liu, Wen-Qian Mao, Jun Yin, Bi-Wen Peng, Wan-Hong Liu, Song Han, Xiao-Hua He

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 30% of its field
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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  4. Identification of Novel Kv1.3 Channel-Interacting Proteins Using Proximity Labelling in T-Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2025
    Article
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  7. Review
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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

10 authors at 1 institution in 1 country.

Xiao-Lu YuanDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Yi-Peng ZhaoDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Jie HuangDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Jun-Chen LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Wen-Qian MaoDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Jun YinDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Bi-Wen PengHubei Provincial Key Laboratory of Developmentally Originated Disease, School of Basic Medical Sciences, Wuhan University, Wuhan, China.ORCID 0000-0002-5599-6779
Wan-Hong LiuHubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Song HanDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.ORCID 0000-0003-4659-4388
Xiao-Hua HeDepartment of Pathophysiology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimMultiple sclerosis (MS) is a neurological autoimmune disorder characterized by mistaken attacks of inflammatory cells against the central nervous system (CNS), resulting in demyelination and axonal damage. Kv1.3 channel blockers can inhibit T-cell activation and have been designed for MS therapy. However, little is known about the effects of Kv1.3 blockers on protecting myelin sheaths/axons in MS. This study aimed at investigating the neuroprotection efficacy of a selective Kv1.3 channel blocker ImKTx88 (ImK) in MS animal model.

methodsExperimental autoimmune encephalomyelitis (EAE) rat model was established. The neuroprotective effect of ImK was assessed by immunohistochemistry and transmission electron microscopy (TEM). In addition, the antiinflammatory effect of ImK by suppressing T-cell activation was assessed by flow cytometry and ELISA in vitro.

resultsOur results demonstrated that ImK administration ameliorated EAE clinical severity. Moreover, ImK increased oligodendrocytes survival, preserved axons, and myelin integrity and reduced the infiltration of activated T cells into the CNS. This protective effect of the peptide may be related to its suppression of autoantigen-specific T-cell activation via calcium influx inhibition.

conclusionImK prevents neurological damage by suppressing T-cell activation, suggesting the applicability of this peptide in MS therapy.

Indexed as

AnimalsAnimals, NewbornCells, CulturedDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleKv1.3 Potassium ChannelMicroscopy, Electron, TransmissionMycobacterium tuberculosisMyelin Basic ProteinNerve Tissue ProteinsNervous System DiseasesNeuronsPotassium Channel BlockersRatsRats, Sprague-DawleyKv1.3 Potassium ChannelMyelin Basic ProteinNerve Tissue ProteinsPotassium Channel BlockersEAEimmunomodulationKv1.3 channelmultiple sclerosisneuroprotection

Identifiers

PMID29577640
PMCPMC6490025
OpenAlexW2793254187

What OpenQuestion holds

Textmetadata
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.