Evidence map›Paper›PMID 37485234›Full record

ArticleBone reports2023

Hypertrophic chondrocytes at the junction of musculoskeletal structures.

Ning Chen, Robin W H Wu, Yan Lam, Wilson C W Chan, Danny Chan

Open access · goldAbstract read
In one paragraph

Article in Bone reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. COX-2 in Fracture Callus Chondro-Osseous Junction Osteoclasts Regulates Chondrocyte Hypertrophy and Callus Vasculogenesis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    Article
  12. Review
  13. International journal of molecular sciences · 2025
    Article
  14. Transcriptomic Profiling of Zebrafish Mutant forInternational journal of molecular sciences · 2025
    Article
  15. Variants inGenetics in medicine open · 2025
    Article
  16. Article
  17. Article
  18. Article
  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

5 authors at 2 institutions in 2 countries.

Ning ChenSchool of Biomedical Sciences, The University of Hong Kong, Hong Kong, China.
Robin W H WuSchool of Biomedical Sciences, The University of Hong Kong, Hong Kong, China.
Yan LamSchool of Biomedical Sciences, The University of Hong Kong, Hong Kong, China.
Wilson C W ChanSchool of Biomedical Sciences, The University of Hong Kong, Hong Kong, China.
Danny ChanSchool of Biomedical Sciences, The University of Hong Kong, Hong Kong, China.
University of Hong Kong · HKUniversity of Hong Kong - Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertrophic chondrocytes are found at unique locations at the junction of skeletal tissues, cartilage growth plate, articular cartilage, enthesis and intervertebral discs. Their role in the skeleton is best understood in the process of endochondral ossification in development and bone fracture healing. Chondrocyte hypertrophy occurs in degenerative conditions such as osteoarthritis. Thus, the role of hypertrophic chondrocytes in skeletal biology and pathology is context dependent. This review will focus on hypertrophic chondrocytes in endochondral ossification, in which they exist in a transient state, but acting as a central regulator of differentiation, mineralization, vascularization and conversion to bone. The amazing journey of a chondrocyte from being entrapped in the extracellular matrix environment to becoming proliferative then hypertrophic will be discussed. Recent studies on the dynamic changes and plasticity of hypertrophic chondrocytes have provided new insights into how we view these cells, not as terminally differentiated but as cells that can dedifferentiate to more progenitor-like cells in a transition to osteoblasts and adipocytes, as well as a source of skeletal stem and progenitor cells residing in the bone marrow. This will provide a foundation for studies of hypertrophic chondrocytes at other skeletal sites in development, tissue maintenance, pathology and therapy.

Indexed as

Cellular plasticityChondrocyte hypertrophyECM remodelingEndochondral ossificationTransdifferentiation

Identifiers

PMID37485234
PMCPMC10359737
OpenAlexW4382933529

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.