Evidence map›Paper›PMID 37626895›Full record

ArticleCells2023

Loss of the Novel Myelin Protein CMTM5 in Multiple Sclerosis Lesions and Its Involvement in Oligodendroglial Stress Responses.

Jiangshan Zhan, Yuanxu Gao, Leo Heinig, Malena Beecken, Yangbo Huo, Wansong Zhang, Pingzhang Wang, Tianzi Wei, Ruilin Tian, Wenling Han and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 26% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. 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

13 authors at 4 institutions in 3 countries.

Jiangshan ZhanSchool of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.ORCID 0000-0002-3836-8332
Yuanxu GaoCenter for Biomedicine and Innovations, Faculty of Medicine, Macau University of Science and Technology, Taipa, Macau 999078, China.ORCID 0000-0001-5314-0195
Leo HeinigInstitute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany.ORCID 0000-0003-4052-7125
Malena BeeckenInstitute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany.
Yangbo HuoSchool of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
Wansong ZhangDepartment of Medical Neuroscience, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.
Pingzhang WangSchool of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
Tianzi WeiDepartment of Medical Neuroscience, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.ORCID 0000-0002-5045-8293
Ruilin TianDepartment of Medical Neuroscience, School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China.
Wenling HanSchool of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
Albert Cheung Hoi YuSchool of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
Markus KippInstitute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany.ORCID 0000-0001-5043-9052
Hannes KaddatzInstitute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, 18057 Rostock, Germany.ORCID 0000-0003-1927-7344
Peking University · CNUniversity of Rostock · DESouthern University of Science and Technology · CNMacau University of Science and Technology · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study comprehensively addresses the involvement of the protein CKLF-like Marvel transmembrane domain-containing family member 5 (CMTM5) in the context of demyelination and cytodegenerative autoimmune diseases, particularly multiple Sclerosis (MS). An observed reduction in CMTM5 expression in post-mortem MS lesions prompted further investigations in both in vitro and in vivo animal models. In the cuprizone animal model, we detected a decrease in CMTM5 expression in oligodendrocytes that is absent in other members of the CMTM protein family. Our findings also confirm these results in the experimental autoimmune encephalomyelitis (EAE) model with decreased CMTM5 expression in both cerebellum and spinal cord white matter. We also examined the effects of a

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisAnimalsAutopsyMiceMyelin ProteinsOligodendrogliaMyelin ProteinsCMTM5cuprizonedemyelinationendoplasmic reticulum stressexperimental autoimmune encephalomyelitismultiple sclerosis

Identifiers

PMID37626895
PMCPMC10453064
OpenAlexW4385949102

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.