Evidence map›Paper›PMID 23897428›Full record

ReviewMolecular and cellular biology2013

The emerging role of p38 mitogen-activated protein kinase in multiple sclerosis and its models.

Dimitry N Krementsov, Tina M Thornton, Cory Teuscher, Mercedes Rincon

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

62 citing papers in PubMed, 108 citations in OpenAlex.

  1. Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Sasanquasaponin fromInternational journal of molecular sciences · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Atypical p38 Signaling, Activation, and Implications for Disease.International journal of molecular sciences · 2021
    Review

2 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Dimitry N KrementsovDepartment of Medicine, Immunobiology Program, University of Vermont, Burlington, Vermont, USA.
Tina M Thornton
Cory Teuscher
Mercedes Rincon
University of Vermont · US

Funding

Vermont Immunobioloigy/ Infectious Diseases CenterP20GM103496 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2012 to 2015
$8.7M
Histamine Receptor Signaling in CNS Autoimmune DiseaseR01NS061014 · NINDS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TEUSCHER, CORY · 2008 to 2012
$3.1M
H1R Signaling and Immune Deviation in EAER01NS069628 · NINDS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TEUSCHER, CORY · 2010 to 2014
$1.6M
p38 MAPK as a female-specific druggable target in CNS autoimmune diseaseR21NS076200 · NINDS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TEUSCHER, CORY · 2011 to 2012
$419k
NIGMS NIH HHS P20 GM103496NINDS NIH HHS R01 NS061014NINDS NIH HHS R01 NS069628NINDS NIH HHS R21 NS076200
6 · The paper itself

Abstract

Multiple sclerosis (MS), the most common disabling neurologic disease of young adults, is considered a classical T cell-mediated disease and is characterized by demyelination, axonal damage, and progressive neurological dysfunction. The currently available disease-modifying therapies are limited in their efficacy, and improved understanding of new pathways contributing to disease pathogenesis could reveal additional novel therapeutic targets. The p38 mitogen-activated protein kinase (MAPK) signaling pathway is known to be triggered by stress stimuli and to contribute to inflammatory responses. Importantly, a number of recent studies have identified this signaling pathway as a central player in MS and its principal animal model, experimental allergic encephalomyelitis. Here, we review the evidence from mouse and human studies supporting the role of p38 MAPK in regulating key immunopathogenic mechanisms underlying autoimmune inflammatory disease of the central nervous system and the potential of targeting this pathway as a disease-modifying therapy in MS.

Indexed as

Disease Models, AnimalAnimalsEncephalomyelitis, Autoimmune, ExperimentalHumansInflammation MediatorsMAP Kinase Signaling SystemMiceModels, ImmunologicalMultiple Sclerosisp38 Mitogen-Activated Protein KinasesInflammation Mediatorsp38 Mitogen-Activated Protein Kinases

Identifiers

PMID23897428
PMCPMC3811866
OpenAlexW2144110754

What OpenQuestion 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 OpenQuestion graph.