Evidence map›Paper›PMID 31847314›Full record

ReviewCells2019

The Role of NF-κB in Physiological Bone Development and Inflammatory Bone Diseases: Is NF-κB Inhibition "Killing Two Birds with One Stone"?

Eijiro Jimi, Nana Takakura, Fumitaka Hiura, Ichiro Nakamura, Shizu Hirata-Tsuchiya

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
4.1field-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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Prenatal Aflatoxin BToxins · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Casticin Inhibits Osteoclastogenesis via NF-κB/BCL-2 Signaling Pathway.Journal of microbiology and biotechnology · 2025
    Article
  18. Article
  19. Article
  20. Article

13 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 1 country.

Eijiro JimiOral Health/Brain Health/Total Health Research Center, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.ORCID 0000-0003-3616-5299
Nana TakakuraLaboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Fumitaka HiuraLaboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
Ichiro NakamuraFaculty of Health and Medical Science, Teikyo Heisei University, 2-51-4 Higashi-Ikebukuro, Toshima, Tokyo 170-8445, Japan.
Shizu Hirata-TsuchiyaDepartment of Biological Endodontics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8553, Japan.ORCID 0000-0003-1520-8587
Kyushu University · JPHiroshima University · JPTeikyo Heisei University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear factor-κB (NF-κB) is a transcription factor that regulates the expression of various genes involved in inflammation and the immune response. The activation of NF-κB occurs via two pathways: inflammatory cytokines, such as TNF-α and IL-1β, activate the "classical pathway", and cytokines involved in lymph node formation, such as CD40L, activate the "alternative pathway". NF-κB1 (p50) and NF-κB2 (p52) double-knockout mice exhibited severe osteopetrosis due to the total lack of osteoclasts, suggesting that NF-κB activation is required for osteoclast differentiation. These results indicate that NF-κB may be a therapeutic target for inflammatory bone diseases, such as rheumatoid arthritis and periodontal disease. On the other hand, mice that express the dominant negative form of IκB kinase (IKK)-β specifically in osteoblasts exhibited increased bone mass, but there was no change in osteoclast numbers. Therefore, inhibition of NF-κB is thought to promote bone formation. Taken together, the inhibition of NF-κB leads to "killing two birds with one stone": it suppresses bone resorption and promotes bone formation. This review describes the role of NF-κB in physiological bone metabolism, pathologic bone destruction, and bone regeneration.

Indexed as

AnimalsBone DevelopmentBone DiseasesBone ResorptionCell DifferentiationCytokinesHumansI-kappa B ProteinsInflammationNF-kappa BOsteoblastsOsteoclastsOsteogenesisSignal TransductionTumor Necrosis Factor-alphaCytokinesI-kappa B ProteinsNF-kappa BTumor Necrosis Factor-alphainflammationNF-κBosteoblastsosteoclasts

Identifiers

PMID31847314
PMCPMC6952937
OpenAlexW2995735301

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.