Evidence map›Paper›PMID 33069239›Full record

ArticleJournal of neuroinflammation2020

Endothelin-1 contributes to the development of virus-induced demyelinating disease.

Young-Hee Jin, Bongsu Kang, Hyun S Kang, Chang-Sung Koh, Byung S Kim

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 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Multiple Sclerosis: Inflammatory and Neuroglial Aspects.Current issues in molecular biology · 2023
    Review
  3. Article
  4. Review
  5. Review
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

5 authors at 2 institutions in 3 countries.

Young-Hee JinDepartment of Microbiology-Immunology, Northwestern University Feinberg Medical School, 303 East Chicago Avenue, Chicago, IL, 60611, USA. jinohee@kiom.re.kr.ORCID http://orcid.org/0000-0001-9916-1418
Bongsu KangDepartment of Microbiology-Immunology, Northwestern University Feinberg Medical School, 303 East Chicago Avenue, Chicago, IL, 60611, USA.
Hyun S KangDepartment of Microbiology-Immunology, Northwestern University Feinberg Medical School, 303 East Chicago Avenue, Chicago, IL, 60611, USA.
Chang-Sung KohDepartment of Biomedical Laboratory Sciences, Graduate School of Medicine, Shinshu University, Matsumoto, Nagano, 390-8621, Japan.
Byung S KimDepartment of Microbiology-Immunology, Northwestern University Feinberg Medical School, 303 East Chicago Avenue, Chicago, IL, 60611, USA. bskim@northwestern.edu.
Northwestern University · USShinshu University · JP

Funding

PATHOGENIC MECHANISMS OF TMEV INDUCED DEMYELINATIONR01NS028752 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KIM, BYUNG S · 1990 to 2008
$2.1M
National Research Council of Science and Technology CRC-16-01-KRICT, NSN1622460NINDS NIH HHS RO1 NS28752, RO1 NS33008
6 · The paper itself

Abstract

backgroundExperimental autoimmune encephalitis (EAE) and virally induced demyelinating disease are two major experimental model systems used to study human multiple sclerosis. Although endothelin-1 level elevation was previously observed in the CNS of mice with EAE and viral demyelinating disease, the potential role of endothelin-1 in the development of these demyelinating diseases is unknown. METHODS AND

resultsIn this study, the involvement of endothelin-1 in the development and progression of demyelinating diseases was investigated using these two experimental models. Administration of endothelin-1 significantly promoted the progression of both experimental diseases accompanied with elevated inflammatory T cell responses. In contrast, administration of specific endothelin-1 inhibitors (BQ610 and BQ788) significantly inhibited progression of these diseases accompanied with reduced T cell responses to the respective antigens.

conclusionsThese results strongly suggest that the level of endothelin-1 plays an important role in the pathogenesis of immune-mediated CNS demyelinating diseases by promoting immune responses.

Indexed as

TheilovirusAnimalsCardiovirus InfectionsDemyelinating DiseasesEndothelin-1FemaleMiceOligopeptidesT-LymphocytesBQ 610Endothelin-1OligopeptidesCNSDemyelinationEAEEndothelin-1TMEV

Identifiers

PMID33069239
PMCPMC7568825
OpenAlexW3092717727

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.