Evidence mapPaperPMID 34310708Full record

ArticleImmunology2021

Vascular and immunopathological role of Asymmetric Dimethylarginine (ADMA) in Experimental Autoimmune Encephalomyelitis.

Inderjit Singh, Judong Kim, Nishant Saxena, Seungho Choi, S M Touhidul Islam, Avtar K Singh, Mushfiquddin Khan, Jeseong Won

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. The Emerging Role of the DDAH Proteins in Psychiatric Disorders.Biological psychiatry global open science · 2025
    Review
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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

8 authors at 1 institution in 1 country.

Inderjit SinghDepartment of Pediatrics, Medical University of South Carolina, Charleston, South Carolina, USA.ORCID 0000-0003-1013-5569
Judong KimDepartment of Pediatrics, Medical University of South Carolina, Charleston, South Carolina, USA.ORCID 0000-0001-5901-689X
Nishant SaxenaDepartment of Pediatrics, Medical University of South Carolina, Charleston, South Carolina, USA.
Seungho ChoiDepartment of Pediatrics, Medical University of South Carolina, Charleston, South Carolina, USA.
S M Touhidul IslamDepartment of Pediatrics, Medical University of South Carolina, Charleston, South Carolina, USA.
Avtar K SinghDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.
Mushfiquddin KhanDepartment of Pediatrics, Medical University of South Carolina, Charleston, South Carolina, USA.ORCID 0000-0001-7945-3237
Jeseong WonDepartment of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.ORCID 0000-0003-2408-0386
Medical University of South Carolina · US

Funding

BLRD VA I01 BX002829
6 · The paper itself

Abstract

Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase (NOS) inhibitor/uncoupler inducing vascular pathology. Vascular pathology is an important factor for the development and progression of CNS pathology of MS, yet the role of ADMA in MS remains elusive. Patients with multiple sclerosis (MS) are reported to have elevated blood levels of ADMA, and mice with experimental autoimmune encephalomyelitis (EAE, an animal model of MS) generated by auto-immunization of myelin oligodendrocyte glycoprotein (MOG) and blood-brain barrier (BBB) disruption by pertussis toxin also had increased blood ADMA levels in parallel with induction of clinical disease. To explore the role of ADMA in EAE pathogenesis, EAE mice were treated with a daily dose of ADMA. It is of special interest that ADMA treatment enhanced the BBB disruption in EAE mice and exacerbated the clinical and CNS disease of EAE. ADMA treatment also induced the BBB disruption and EAE disease in MOG-immunized mice even without pertussis toxin treatment, suggesting the role of ADMA in BBB dysfunction in EAE. T-cell polarization studies also documented that ADMA treatment promotes T

Indexed as

AnimalsArginineBlood-Brain BarrierCD4-Positive T-LymphocytesEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansMiceMultiple SclerosisMyelin-Oligodendrocyte GlycoproteinPertussis ToxinArginineMog protein, mouseMyelin-Oligodendrocyte GlycoproteinN,N-dimethylargininePertussis ToxinAsymmetric dimethylarginine (ADMA)blood-brain barrier (BBB)experimental autoimmune encephalomyelitis (EAE)multiple sclerosismyelinTH1TH17T helper lymphocytesvascular pathology

Identifiers

PMID34310708
PMCPMC8517583
OpenAlexW3184961867

What Socratic holds

Textmetadata
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.