Evidence map›Paper›PMID 34220419›Full record

ArticleFrontiers in neuroscience2021

The Function of the Hypothalamic-Pituitary-Adrenal Axis During Experimental Autoimmune Encephalomyelitis: Involvement of Oxidative Stress Mediators.

Svetlana Trifunovic, Ivana Stevanovic, Ana Milosevic, Natasa Ristic, Marija Janjic, Ivana Bjelobaba, Danijela Savic, Iva Bozic, Marija Jakovljevic, Katarina Tesovic and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

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  13. Oxidative Stress Markers in Multiple Sclerosis.International journal of molecular sciences · 2024
    Review
  14. Experimental Autoimmune Encephalomyelitis Influences GH-Axis in Female Rats.International journal of molecular sciences · 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

12 authors at 2 institutions in 1 country.

Svetlana TrifunovicInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Ivana StevanovicMedical Faculty of Military Medical Academy, Institute of Medical Research Belgrade, University of Defense, Belgrade, Serbia.
Ana MilosevicInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Natasa RisticInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Marija JanjicInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Ivana BjelobabaInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Danijela SavicInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Iva BozicInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Marija JakovljevicInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Katarina TesovicInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Danijela LaketaDepartment for General Physiology and Biophysics, Faculty of Biology, University of Belgrade, Belgrade, Serbia.
Irena LavrnjaInstitute for Biological Research "Siniša Stanković"-National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia.
University of Belgrade · RSMilitary Medical Academy · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is an inflammatory, demyelinating disease with an unknown origin. Previous studies showed the involvement of the hypothalamic-pituitary-adrenal (HPA) axis to susceptibility to autoimmune diseases, including MS, and its best-characterized animal model, experimental autoimmune encephalomyelitis (EAE). During MS/EAE, innate immune cells are activated and release cytokines and other inflammatory mediators, leading to a vicious cycle of inflammation. In response to inflammation, the activated HPA axis modulates immune responses

Indexed as

cytokinesexperimental autoimmune encephalomyelitishypothalamic–pituitary–adrenal axismultiple sclerosisoxidative stress

Identifiers

PMID34220419
PMCPMC8248369
OpenAlexW3177254717

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.