Evidence map›Paper›PMID 36499018›Full record

ArticleInternational journal of molecular sciences2022

Blockade of Kv1.3 Potassium Channel Inhibits Microglia-Mediated Neuroinflammation in Epilepsy.

Xinyi Zhang, Peiyu Liang, Yahui Zhang, Yifan Wu, Yinghao Song, Xueyang Wang, Taoxiang Chen, Biwen Peng, Wanhong Liu, Jun Yin and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Frontiers in pharmacology · 2023
    Article
  16. Newly IdentifiedEpilepsy currents
    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 at 1 institution in 1 country.

Xinyi ZhangDepartment of Pathophysiology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Peiyu LiangDepartment of Pathophysiology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Yahui ZhangDepartment of Pathophysiology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Yifan WuDepartment of Pathophysiology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Yinghao SongDepartment of Pathophysiology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Xueyang WangDepartment of Pathophysiology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Taoxiang ChenHubei Provincial Key Laboratory of Developmentally Originated Disease, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Biwen PengHubei Provincial Key Laboratory of Developmentally Originated Disease, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Wanhong LiuDepartment of Immunology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Jun YinDepartment of Pathophysiology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Song HanDepartment of Pathophysiology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.ORCID 0000-0003-4659-4388
Xiaohua HeDepartment of Pathophysiology, Taikang Medical School (School of Basic Medical Sciences), Wuhan University, Wuhan 430071, China.
Wuhan University · CN

Funding

Medical Science Advancement Program of Wuhan University TFJC2018001Medical Science Advancement Program of Wuhan University TFLC2018001National Natural Science Foundation of China 82171451Translational Medicine and Interdisciplinary Research Joint Fund of Zhongnan Hospital of Wuhan University ZNLH201909
6 · The paper itself

Abstract

Epilepsy is a chronic neurological disorder whose pathophysiology relates to inflammation. The potassium channel Kv1.3 in microglia has been reported as a promising therapeutic target in neurological diseases in which neuroinflammation is involved, such as multiple sclerosis (MS), Alzheimer's disease (AD), Parkinson's disease (PD), and middle cerebral artery occlusion/reperfusion (MCAO/R). Currently, little is known about the relationship between Kv1.3 and epilepsy. In this study, we found that Kv1.3 was upregulated in microglia in the KA-induced mouse epilepsy model. Importantly, blocking Kv1.3 with its specific small-molecule blocker 5-(4-phenoxybutoxy)psoralen (PAP-1) reduced seizure severity, prolonged seizure latency, and decreased neuronal loss. Mechanistically, we further confirmed that blockade of Kv1.3 suppressed proinflammatory microglial activation and reduced proinflammatory cytokine production by inhibiting the Ca

Indexed as

EpilepsyKv1.3 Potassium ChannelAnimalsDisease Models, AnimalMiceMicrogliaSeizuresKv1.3 Potassium ChannelcalciumepilepsyinflammationKv1.3microgliaNF-κB signaling pathway

Identifiers

PMID36499018
PMCPMC9740890
OpenAlexW4310038872

What OpenQuestion holds

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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.