Evidence map›Paper›PMID 32197115›Full record

ArticleStem cell reports2020

Expansion of Bone Precursors through Jun as a Novel Treatment for Osteoporosis-Associated Fractures.

Tristan Lerbs, Lu Cui, Claire Muscat, Atif Saleem, Camille van Neste, Pablo Domizi, Charles Chan, Gerlinde Wernig

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 22 citations in OpenAlex.

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  16. Inherited Defects of the ASC-1 Complex in Congenital Neuromuscular Diseases.International journal of molecular sciences · 2021
    Review
  17. Network Pharmacological Study ofBioMed research international · 2021
    Article
  18. Article
  19. 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

8 authors at 1 institution in 1 country.

Tristan LerbsDepartment of Pathology, Stanford School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA.
Lu CuiDepartment of Pathology, Stanford School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA.
Claire MuscatDepartment of Pathology, Stanford School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA.
Atif SaleemDepartment of Pathology, Stanford School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA.
Camille van NesteDepartment of Pathology, Stanford School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA.
Pablo DomiziDepartment of Pathology, Stanford School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA.
Charles ChanInstitute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305, USA; Department of Plastic and Reconstructive Surgery, Stanford School of Medicine, Stanford, CA 94305, USA.
Gerlinde WernigDepartment of Pathology, Stanford School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford School of Medicine, Stanford, CA 94305, USA. Electronic address: gwernig@stanford.edu.
Stanford Medicine · US

Funding

Immune Checkpoint Inhibitors as Antifibrotic Therapy for Idiopathic Pulmonary FibrosisK08HL143143 · NHLBI · STANFORD UNIVERSITY · PI WERNIG, GERLINDE · 2018 to 2020
$502k
NHLBI NIH HHS K08 HL143143
6 · The paper itself

Abstract

Osteoporosis and osteoporotic fractures lead to decreased life quality and high healthcare costs. Current treatments prevent losses in bone mass and fractures to some extent but have side effects. Therefore, better therapies are needed. This study investigated whether the transcription factor Jun has a specific pro-osteogenic potency and whether modulating Jun could serve as a novel treatment for osteoporosis-associated fractures. We demonstrate that ectopically transplanted whole bones and distinct osteoprogenitors increase bone formation. Perinatal Jun induction disturbs growth plate architecture, causing a striking phenotype with shortened and thickened bones. Molecularly, Jun induces hedgehog signaling in skeletal stem cells. Therapeutically, Jun accelerates bone growth and healing in a drilling-defect model. Altogether, these results demonstrate that Jun drives bone formation by expanding osteoprogenitor populations and forcing them into the bone fate, providing a rationale for future clinical applications.

Indexed as

AnimalsBone and BonesBone DevelopmentBone TransplantationCell DifferentiationCell ProliferationFracture HealingGrowth PlateHedgehog ProteinsMiceOsteoporotic FracturesPhenotypeProto-Oncogene Proteins c-junSignal TransductionStem CellsHedgehog ProteinsProto-Oncogene Proteins c-junbone precursor expansionbone precursorsfracturesJUNosteoporosisosteoprogenitorsskeletal stem cellsstem cell therapy

Identifiers

PMID32197115
PMCPMC7160304
OpenAlexW3012189438

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.