Evidence map›Paper›PMID 23963632›Full record

ReviewCalcified tissue international2014

Notch signaling in skeletal stem cells.

Shan Chen, Brendan H Lee, Yangjin Bae

Open access · greenAbstract readReview
In one paragraph

Review in Calcified tissue international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Role of Notch signaling pathway in joint homeostasis and osteoarthritis.Frontiers in bioengineering and biotechnology · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Research advances in cartilage stem cells markers and induced differentiation.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Enthesis regeneration: a role for Gli1+ progenitor cells.Development (Cambridge, England) · 2017
    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

3 authors at 1 institution in 1 country.

Shan ChenDepartment of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza Rm R814, Houston, TX, 77030, USA.
Brendan H Lee
Yangjin Bae
Baylor College of Medicine · US

Funding

UNDERSTANDING FXTAS AMONG MALES WITH THE FMR1 PREMUTATIONP30HD024064 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI TOLIAS, KIMBERLY R · 1988 to 2013
$29.4M
THE SKELETAL DYSPLASIASP01HD022657 · NICHD · CEDARS-SINAI MEDICAL CENTER · PI LEE, BRENDAN · 1987 to 2011
$17.0M
Project 3: Collagen post-translational modification and cross-linking in OIP01HD070394 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI LEE, BRENDAN · 2011 to 2020
$13.4M
Mouse mutations that model human craniofacial/limb abnormalitiesP01ES011253 · NIEHS · BAYLOR COLLEGE OF MEDICINE · PI LEE, BRENDAN HL · 2001 to 2005
$5.4M
Transcriptional Regulation of Craniofacial SkeletogenesisR01DE016990 · NIDCR · BAYLOR COLLEGE OF MEDICINE · PI LEE, BRENDAN · 2005 to 2009
$1.6M
Dysregulation of 3-prolyl-hydroxylation in Human Skeletal DysplasiasR01DE017713 · NIDCR · BAYLOR COLLEGE OF MEDICINE · PI LEE, BRENDAN · 2006 to 2010
$836k
Howard Hughes Medical InstituteNICHD NIH HHS HD022657NICHD NIH HHS P01 HD022657NICHD NIH HHS P01 HD070394NICHD NIH HHS P30 HD024064NIDCR NIH HHS DE016990NIDCR NIH HHS R01 DE016990NIDCR NIH HHS R01 DE017713NIEHS NIH HHS P01 ES011253
6 · The paper itself

Abstract

The skeleton originates from stem cells residing in the sclerotome and neural crest that undergo proliferation, migration, and commitment. The development of the skeletal stem cells is influenced by many signaling pathways that govern cell fate determination, proliferation, differentiation, and apoptosis. This review will focus on Notch signaling functions in regulating the different cell types that form the skeletal system as well as the interplay between them to maintain homeostasis. Osteochondroprogenitors require Notch signaling to maintain multipotency and to prevent premature differentiation into osteoblasts. Subsequently, overactivation of Notch signaling suppresses osteoblast maturation. Moreover, Notch signaling in osteochondroprogenitors is required for chondrocyte proliferation and hypertrophy and suppresses terminal differentiation. Translational studies demonstrated a crucial role of Notch signaling in osteosarcoma and osteoarthritis, where concepts derived from developmental pathways are often recapitulated. This brings hope of taking advantage of the molecular mechanisms learned from development to approach the pathological processes underlying abnormal bone/cartilage metabolism or tumorigenesis. Pharmacological agents that target Notch receptors or ligands in a tissue-specific fashion would offer new opportunities for treating bone/cartilage diseases caused by dysregulation of Notch signaling.

Indexed as

AnimalsBone and BonesCell DifferentiationHumansMuscle, SkeletalReceptors, NotchSignal TransductionStem CellsReceptors, Notch

Identifiers

PMID23963632
PMCPMC3947214
OpenAlexW1992289603

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.