Evidence map›Paper›PMID 20199390›Full record

ReviewCurrent drug targets2010

NF-kappaB signaling: multiple angles to target OA.

Kenneth B Marcu, Miguel Otero, Eleonora Olivotto, Rosa Maria Borzi, Mary B Goldring

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 286 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
286citing papers in PubMed, 4 pooled it
20.7field-weighted citation impact, top 1% 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

286 citing papers in PubMed, 4 syntheses or guidelines pooled it, 555 citations in OpenAlex.

  1. Pooled it
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  4. Efficacy and Safety of Curcumin andFrontiers in immunology · 2022
    Pooled it
  5. Trial
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  17. International journal of medical sciences · 2026
    Article
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  19. Edible HerbInternational journal of molecular sciences · 2025
    Article
  20. Article

226 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

5 authors at 3 institutions in 2 countries.

Kenneth B MarcuBiochemistry and Cell Biology Department, Stony Brook University, Stony Brook, NY 11794, USA. kenneth.marcu@stonybrook.edu
Miguel Otero
Eleonora Olivotto
Rosa Maria Borzi
Mary B Goldring
Hospital for Special Surgery · USIstituto Ortopedico Rizzoli · ITStony Brook University · US

Funding

Defining Common Molecular Parameters For Onset and Progression of OsteoarthritisRC4AR060546 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI GOLDRING, MARY B, LI, YEFU · 2010 to 2010
$4.1M
Role of ESE1 Regulation of Type II Collagen in CartilageR01AG022021 · NIA · HOSPITAL FOR SPECIAL SURGERY · PI GOLDRING, MARY B · 2002 to 2014
$3.4M
Novel roles of IKK complex to program gene expressionR01GM066882 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI MARCU, KENNETH B · 2003 to 2006
$1.3M
ESE 1 a novel transcriptional regulator of cartilage remodelingR56AG022021 · NIA · HOSPITAL FOR SPECIAL SURGERY · PI GOLDRING, MARY B · 2009 to 2009
$438k
Epigenetic Regulation of MMP-13R21AR054887 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI GOLDRING, MARY B · 2007 to 2008
$355k
NIAMS NIH HHS R21 AR054887NIAMS NIH HHS R21-AR054887NIAMS NIH HHS RC4 AR060546NIA NIH HHS AG022021NIA NIH HHS R01 AG022021NIA NIH HHS R56 AG022021NIGMS NIH HHS GM066882NIGMS NIH HHS R01 GM066882
6 · The paper itself

Abstract

In the context of OA disease, NF-kappaB transcription factors can be triggered by a host of stress-related stimuli including pro-inflammatory cytokines, excessive mechanical stress and ECM degradation products. Activated NF-kappaB regulates the expression of many cytokines and chemokines, adhesion molecules, inflammatory mediators, and several matrix degrading enzymes. NF-kappaB also influences the regulated accumulation and remodeling of ECM proteins and has indirect positive effects on downstream regulators of terminal chondrocyte differentiation (including beta-catenin and Runx2). Although driven partly by pro-inflammatory and stress-related factors, OA pathogenesis also involves a "loss of maturational arrest" that inappropriately pushes chondrocytes towards a more differentiated, hypertrophic-like state. Growing evidence points to NF-kappaB signaling as not only playing a central role in the pro-inflammatory stress-related responses of chondrocytes to extra- and intra-cellular insults, but also in the control of their differentiation program. Thus unlike other signaling pathways the NF-kappaB activating kinases are potential therapeutic OA targets for multiple reasons. Targeted strategies to prevent unwanted NF-kappaB activation in this context, which do not cause side effects on other proteins or signaling pathways, need to be focused on the use of highly specific drug modalities, siRNAs or other biological inhibitors that are targeted to the activating NF-kappaB kinases IKKalpha or IKKbeta or specific activating canonical NF-kappaB subunits. However, work remains in its infancy to evaluate the effects of efficacious, targeted NF-kappaB inhibitors in animal models of OA disease in vivo and to also target these strategies only to affected cartilage and joints to avoid other undesirable systemic effects.

Indexed as

AnimalsAnti-Inflammatory AgentsCell DifferentiationChondrocytesDrug Delivery SystemsHumansI-kappa B KinaseModels, BiologicalNF-kappa BOsteoarthritisSignal TransductionAnti-Inflammatory AgentsI-kappa B KinaseNF-kappa B

Identifiers

PMID20199390
PMCPMC3076145
OpenAlexW2132612143

What OpenQuestion holds

Textmetadata
LicenceTDM
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.