Evidence map›Paper›PMID 34666785›Full record

ArticleJournal of neuroinflammation2021

Inhibition of lysophosphatidic acid receptor 1-3 deteriorates experimental autoimmune encephalomyelitis by inducing oxidative stress.

Jong Hee Choi, Jinhee Oh, Min Jung Lee, Hyunsu Bae, Seong-Gyu Ko, Seung-Yeol Nah, Ik-Hyun Cho

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. A combined extract ofJournal of ginseng research · 2026
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  4. Non-saponin fromJournal of ginseng research · 2025
    Article
  5. Review
  6. NADPH Oxidase 3: Beyond the Inner Ear.Antioxidants (Basel, Switzerland) · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Gintonin, aJournal of ginseng research · 2023
    Article
  11. Article
  12. 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

7 authors at 2 institutions in 1 country.

Jong Hee ChoiDepartment of Convergence Korean Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea.
Jinhee OhDepartment of Convergence Korean Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea.
Min Jung LeeDepartment of Convergence Korean Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea.
Hyunsu BaeDepartment of Physiology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea.
Seong-Gyu KoKorean Medicine-Based Drug Repositioning Cancer Research Center, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea.
Seung-Yeol NahGinsentology Research Laboratory and Department of Physiology, College of Veterinary Medicine and Bio/Molecular Informatics Center, Konkuk University, Seoul, 05029, Republic of Korea.
Ik-Hyun ChoDepartment of Convergence Korean Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea. ihcho@khu.ac.kr.ORCID http://orcid.org/0000-0002-3868-7384
Kyung Hee University · KRKonkuk University · KR

Funding

Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, and ICT 2017R1A2A2A05069493Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, and ICT NRF-2016M3C7A1905074Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, and ICT NRF-2020R1A5A2019413Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, and ICT NRF-2021R1H1A2010055
6 · The paper itself

Abstract

backgroundLysophosphatidic acid receptors (LPARs) are G-protein-coupled receptors involved in many physiological functions in the central nervous system. However, the role of the LPARs in multiple sclerosis (MS) has not been clearly defined yet.

methodsHere, we investigated the roles of LPARs in myelin oligodendrocyte glycoprotein peptides-induced experimental autoimmune encephalomyelitis (EAE), an animal model of MS.

resultsPre-inhibition with LPAR1-3 antagonist Ki16425 deteriorated motor disability of EAE

conclusionsOur findings strongly suggest that some agents that can stimulate LPARs might have potential therapeutic implications for autoimmune demyelinating diseases such as MS.

Indexed as

AnimalsDose-Response Relationship, DrugEncephalomyelitis, Autoimmune, ExperimentalFemaleIsoxazolesMiceMice, Inbred C57BLMyelin-Oligodendrocyte GlycoproteinOxidative StressPeptide FragmentsPropionatesReceptors, Lysophosphatidic Acid3-(4-(4-((1-(2-chlorophenyl)ethoxy)carbonyl amino)-3-methyl-5-isoxazolyl) benzylsulfanyl) propanoic acidIsoxazolesLPAR1 protein, mouseLPAR2 protein, humanLpar3 protein, mouseMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsPropionatesReceptors, Lysophosphatidic AcidExperimental autoimmune encephalomyelitisLysophosphatidic acid receptorsNADPH oxidaseReactive oxygen species

Identifiers

PMID34666785
PMCPMC8527776
OpenAlexW3111592312

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.