Evidence map›Paper›PMID 28467798›Full record

ArticleOncotarget2017

Mechanism of oxidative stress p38MAPK-SGK1 signaling axis in experimental autoimmune encephalomyelitis (EAE).

Liang Wang, Bin Li, Mo-Yuan Quan, Lin Li, Yuan Chen, Guo-Jun Tan, Jing Zhang, Xiao-Peng Liu, Li Guo

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Celastrol suppresses experimental autoimmune encephalomyelitis via MAPK/SGK1-regulated mediators of autoimmune pathology.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
  18. Review
  19. 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

9 authors at 3 institutions in 1 country.

Liang WangDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Bin LiDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Mo-Yuan QuanDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Lin LiDepartment of Neurology, Tongren Hospital of Capital Medical University, Beijing, Hebei 100088, China.
Yuan ChenDepartment of Pediatrics, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Guo-Jun TanDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Jing ZhangDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Xiao-Peng LiuDepartment of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Li GuoDepartment of Neurology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China.
Hebei Medical University · CNSecond Hospital of Hebei Medical University · CNBeijing Tongren Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultiple sclerosis (MS), a complex disease associated with multifocal demyelination of the central nervous system and poorly understood etiology. It has been previously indicated that many factors, including oxidative stress and p38MAPK-SGK1 pathway, contribute to the pathogenesis of MS.

methodsThis study, using an experimental autoimmune encephalomyelitis (EAE) model system, was aimed at investigating the molecular mechanisms determining interaction p38MAPK-SGK1 pathway and oxidative stress in MS pathogenesis. C57BL/6 mice was immunized with MOG35-55 peptide for EAE induction, which was followed by determination of the effect of treatment with classic p38 inhibitor SB203580 and antioxidant tempol on the development and progression of EAE.

resultsOur experiments showed a dynamic change of immune inflammation, oxidative stress and p38MAPK-SGK1 pathway involvement in EAE demonstrating that p38MAPK-SGK1 pathway and oxidative stress contribute to the demyelination in central nerve system caused by Th17 inflammatory responses in a synergistic way. The administration of SB203580 and Tempol both markedly suppressed the progression of EAE. Furthermore, tempol showed a strong inhibiting effect to the p38MAPK-SGK1 pathway similar to SB203580 suggesting that oxidative stress exacerbates EAE via the activation of p38MAPK-SGK1 pathway.

conclusionCumulatively, our results show that oxidative stress p38MAPK-SGK1 signaling pathway may be a central player in EAE and even in MS.

Indexed as

MAP Kinase Signaling SystemAnimalsEncephalomyelitis, Autoimmune, ExperimentalFemaleImmediate-Early ProteinsMiceMice, Inbred C57BLOxidative Stressp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesSerum-Glucocorticoid Regulated KinasesImmediate-Early Proteinsp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesSerum-Glucocorticoid Regulated KinasesEAEmultiple sclerosisoxidative stressp38MAPK-SGK1

Identifiers

PMID28467798
PMCPMC5522107
OpenAlexW2605610044

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.