Evidence map›Paper›PMID 33158440›Full record

ArticleJournal of neuroinflammation2020

Deficiency of microglial Hv1 channel is associated with activation of autophagic pathway and ROS production in LPC-induced demyelination mouse model.

Man Chen, Lin-Lin Yang, Zi-Wei Hu, Chuan Qin, Luo-Qi Zhou, Ya-Ling Duan, Dale B Bosco, Long-Jun Wu, Ke-Bin Zhan, Sha-Bei Xu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  6. Erk5-mediated microglial ferroptosis drives ischemic white matter damage via the Nfatc4-Clptm1l axis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  8. Review
  9. Validation of HvFrontiers in cellular neuroscience · 2025
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  13. Review
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  15. Inhibition of the HFrontiers in immunology · 2024
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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

11 authors at 3 institutions in 2 countries.

Man ChenDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People's Republic of China.
Lin-Lin YangDepartment of Neurology, Second Affiliated Hospital of University of South China, Hengyang, 421001, Hunan, People's Republic of China.
Zi-Wei HuDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People's Republic of China.
Chuan QinDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People's Republic of China.
Luo-Qi ZhouDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People's Republic of China.
Ya-Ling DuanDepartment of Neurology, Second Affiliated Hospital of University of South China, Hengyang, 421001, Hunan, People's Republic of China.
Dale B BoscoDepartment of Neurology, Mayo Clinic, Rochester, MN, 55905, USA.
Long-Jun WuDepartment of Neurology, Mayo Clinic, Rochester, MN, 55905, USA.
Ke-Bin ZhanDepartment of Neurology, Second Affiliated Hospital of University of South China, Hengyang, 421001, Hunan, People's Republic of China. zhankebin@126.com.
Sha-Bei XuDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People's Republic of China. xushabei@126.com.
Dai-Shi TianDepartment of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People's Republic of China. tiands@tjh.tjmu.edu.cn.ORCID http://orcid.org/0000-0002-7627-0811
Tongji Hospital · CNUniversity of South China · CNMayo Clinic · US

Funding

National Natural Science Foundation of China 81571132, 81873743
6 · The paper itself

Abstract

backgroundMultiple sclerosis (MS) is an immune-mediated demyelinated disease of the central nervous system. Activation of microglia is involved in the pathogenesis of myelin loss.

objectiveThis study is focused on the role of Hv1 in regulating demyelination and microglial activation through reactive oxygen species (ROS) production after lysophosphatidylcholine (LPC)-mediated demyelination. We also explored autophagy in this process.

methodsA model of demyelination using two-point LPC injection into the corpus callosum was established. LFB staining, immunofluorescence, Western blot, and electron microscopy were used to study the severity of demyelination. Microglial phenotype and autophagy were detected by immunofluorescence and Western blot. Morris water maze was used to test spatial learning and memory ability.

resultsWe have identified that LPC-mediated myelin damage was reduced by Hv1 deficiency. Furthermore, we found that ROS and autophagy of microglia increased in the demyelination region, which was also inhibited by Hv1 knockout.

conclusionThese results suggested that microglial Hv1 deficiency ameliorates demyelination through inhibition of ROS-mediated autophagy and microglial phenotypic transformation.

Indexed as

AnimalsAutophagyDemyelinating DiseasesDisease Models, AnimalFemaleIon ChannelsLysophosphatidylcholinesMaleMiceMice, Inbred C57BLMice, KnockoutMicrogliaReactive Oxygen SpeciesHv1 proton channel, mouseIon ChannelsLysophosphatidylcholinesReactive Oxygen SpeciesAutophagyDemyelinationMicrogliaNeuroinflammationROS

Identifiers

PMID33158440
PMCPMC7646080
OpenAlexW3097130862

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.