Evidence map›Paper›PMID 17947700›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2007

Biomechanical signals suppress TAK1 activation to inhibit NF-kappaB transcriptional activation in fibrochondrocytes.

Shashi Madhavan, Mirela Anghelina, Danen Sjostrom, Anar Dossumbekova, Denis C Guttridge, Sudha Agarwal

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. TNFα-Related Chondrocyte Inflammation Models: A Systematic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Review
  3. Frontiers in bioengineering and biotechnology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Mechanosignaling in bone health, trauma and inflammation.Antioxidants & redox signaling · 2014
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Mechanical intervention for maintenance of cartilage and bone.Clinical medicine insights. Arthritis and musculoskeletal disorders · 2011
    Article
  19. Article
  20. 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

6 authors at 3 institutions in 3 countries.

Shashi MadhavanBiomechanics and Tissue Engineering Laboratory, Section of Oral Biology, Ohio State University, Columbus 43210, USA.
Mirela Anghelina
Danen Sjostrom
Anar Dossumbekova
Denis C Guttridge
Sudha Agarwal
Biomechanics Institute of Valencia · ESDepartment of Virology · FRThe Ohio State University · US

Funding

Exercise Driven Molecular Mechanisms of Joint RepairR01AR048781 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AGARWAL, SUDHA · 2002 to 2006
$1.5M
Inflammation of TMJDs: Role of Biomechanical SignalsR01DE015399 · NIDCR · OHIO STATE UNIVERSITY · PI AGARWAL, SUDHA · 2003 to 2006
$1.4M
STRESS-INDUCED ANTI-INFLAMMATORY SIGNALS IN CHONDROCYTESR01AT000646 · NCCIH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AGARWAL, SUDHA · 2000 to 2004
$1.1M
Physical Therapy, An Antiflammatory Signal on ArthritisR21HD040939 · NICHD · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AGARWAL, SUDHA · 2001 to 2004
$655k
NCCIH NIH HHS AT00646NCCIH NIH HHS R01 AT000646NIAMS NIH HHS AR04878NIAMS NIH HHS R01 AR048781NICHD NIH HHS HD40939NICHD NIH HHS R21 HD040939NIDCR NIH HHS DE15399NIDCR NIH HHS R01 DE015399
6 · The paper itself

Abstract

Exercise/joint mobilization is therapeutic for inflammatory joint diseases like rheumatoid and osteoarthritis, but the mechanisms underlying its actions remain poorly understood. We report that biomechanical signals at low/physiological magnitudes are potent inhibitors of inflammation induced by diverse proinflammatory activators like IL-1beta, TNF-alpha, and lipopolysaccharides, in fibrochondrocytes. These signals exert their anti-inflammatory effects by inhibiting phosphorylation of TAK1, a critical point where signals generated by IL-1beta, TNF-alpha, and LPS converge to initiate NF-kappaB signaling cascade and proinflammatory gene induction. Additionally, biomechanical signals inhibit multiple steps in the IL-1beta-induced proinflammatory cascade downstream of IkappaB kinase activation to regulate IkappaBalpha and IkappaBbeta degradation and synthesis, and promote IkappaBalpha shuttling to export nuclear NF-kappaB and terminate its transcriptional activity. The findings demonstrate that biomechanical forces are but another important signal that uses NF-kappaB pathway to regulate inflammation by switching the molecular activation of discrete molecules involved in proinflammatory gene transcription.

Indexed as

Signal TransductionActive Transport, Cell NucleusAnimalsBiomechanical PhenomenaCells, CulturedChondrocytesEnzyme ActivationFemaleGene Expression Regulation, EnzymologicI-kappa B KinaseInterleukin-1betaLipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMatrix Metalloproteinase 13NF-kappa BI-kappa B KinaseInterleukin-1betaLipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMatrix Metalloproteinase 13NF-kappa BNitric Oxide Synthase Type IINos2 protein, ratTumor Necrosis Factor-alpha

Identifiers

PMID17947700
PMCPMC4950928
OpenAlexW2099624801

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.