Evidence map›Paper›PMID 28955690›Full record

ReviewJournal of bone metabolism2017

Regulation of Cartilage Development and Diseases by Transcription Factors.

Riko Nishimura, Kenji Hata, Yoshifumi Takahata, Tomohiko Murakami, Eriko Nakamura, Hiroko Yagi

Open access · greenAbstract readReview
In one paragraph

Review in Journal of bone metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  9. Association ofOpen medicine (Warsaw, Poland) · 2024
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  12. Article
  13. Review
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  16. RUNX3 Polymorphisms Affect the Risk of Ankylosing Spondylitis.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  17. Article
  18. Review
  19. Article
  20. Article
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 1 institution in 1 country.

Riko NishimuraDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Kenji HataDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Yoshifumi TakahataDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Tomohiko MurakamiDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Eriko NakamuraDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Hiroko YagiDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, Osaka, Japan.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic studies and molecular cloning approaches have been successfully used to identify several transcription factors that regulate the numerous stages of cartilage development. Sex-determining region Y (SRY)-box 9 (Sox9) is an essential transcription factor for the initial stage of cartilage development. Sox5 and Sox6 play an important role in the chondrogenic action of Sox9, presumably by defining its cartilage specificity. Several transcription factors have been identified as transcriptional partners for Sox9 during cartilage development. Runt-related transcription factor 2 (Runx2) and Runx3 are necessary for hypertrophy of chondrocytes. CCAAT/enhancer-binding protein β (C/EBPβ) and activating transcription factor 4 (ATF4) function as co-activators for Runx2 during hypertrophy of chondrocytes. In addition, myocyte-enhancer factor 2C (Mef2C) is required for initiation of chondrocyte hypertrophy, presumably by functioning upstream of Runx2. Importantly, the pathogenic roles of several transcription factors in osteoarthritis have been demonstrated based on the similarity of pathological phenomena seen in osteoarthritis with chondrocyte hypertrophy. We discuss the importance of investigating cellular and molecular properties of articular chondrocytes and degradation mechanisms in osteoarthritis, one of the most common cartilage diseases.

Indexed as

CartilageChondrocytesOsteoarthritisTranscription factors

Identifiers

PMID28955690
PMCPMC5613019
OpenAlexW2757904165

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.