Evidence map›Paper›PMID 23028406›Full record

ArticleThe open rheumatology journal2012

The p38 MAPK Pathway in Rheumatoid Arthritis: A Sideways Look.

Andrew R Clark, Jonathan LE Dean

Open access · hybridAbstract read
In one paragraph

Article in The open rheumatology journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Molecular insights into phytochemicals exhibiting anti-arthritic activity: systematic review : John Di Battista.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Pooled it
  2. Therapeutic potential of zinc supplementation in rheumatoid arthritis: clinical evidence, molecular mechanisms, and formulation-specific effects.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Studying molecular signaling in major angiogenic diseases.Molecular and cellular biochemistry · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. RA-map: building a state-of-the-art interactive knowledge base for rheumatoid arthritis.Database : the journal of biological databases and curation · 2020
    Article
  16. Article
  17. Article
  18. Review
  19. A Network Pharmacology Study on the Active Ingredients and Potential Targets ofEvidence-based complementary and alternative medicine : eCAM · 2019
    Article
  20. Roles of Mitogen-Activated Protein Kinases in Osteoclast Biology.International journal of molecular sciences · 2018
    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

2 authors at 1 institution in 1 country.

Andrew R ClarkKennedy Institute of Rheumatology Division, Imperial College London, 65 Aspenlea Road, Hammersmith, London W6 8LH, UK.
Jonathan LE Dean
Hammersmith Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p38 mitogen-activated protein kinase (MAPK) signaling pathway has been strongly implicated in many of the processes that underlie the pathology of rheumatoid arthritis (RA). For many years it has been considered a promising target for development of new anti-inflammatory drugs with which to treat RA and other chronic immune-mediated inflammatory diseases. However, several recent clinical trials have concluded in a disappointing manner. Why is this so, if p38 MAPK clearly contributes to the excessive production of inflammatory mediators, the destruction of bone and cartilage? We argue that, to explain the apparent failure of p38 inhibitors in the rheumatology clinic, we need to understand better the complexities of the p38 pathway and its many levels of communication with other cellular signaling pathways. In this review we look at the p38 MAPK pathway from a slightly different perspective, emphasising its role in post-transcriptional rather than transcriptional control of gene expression, and its contribution to the off-phase rather than the on-phase of the inflammatory response.

Identifiers

PMID23028406
PMCPMC3460412
OpenAlexW2006344722

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.