Evidence map›Paper›PMID 29868574›Full record

ReviewFrontiers in bioengineering and biotechnology2018

Microenvironmental Regulation of Chondrocyte Plasticity in Endochondral Repair-A New Frontier for Developmental Engineering.

Sarah A Wong, Kevin O Rivera, Theodore Miclau, Eben Alsberg, Ralph S Marcucio, Chelsea S Bahney

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in bioengineering and biotechnology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

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  13. Activation of canonical Wnt signaling accelerates intramembranous bone regeneration in male mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022
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  17. Chondrocyte-to-osteoblast transformation in mandibular fracture repair.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2021
    Article
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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 2 institutions in 1 country.

Sarah A WongDepartment of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States.
Kevin O RiveraDepartment of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States.
Theodore MiclauDepartment of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States.
Eben AlsbergDepartment of Orthopaedic Surgery and Biomedical Engineering, Case Western Reserve University, Cleveland, OH, United States.
Ralph S MarcucioDepartment of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States.
Chelsea S BahneyDepartment of Orthopaedic Surgery, Orthopaedic Trauma Institute, University of California, San Francisco, San Francisco, CA, United States.
University of California, San Francisco · USCase Western Reserve University · US

Funding

Engaging University of California Stakeholders for Biorespository ResearchUL1TR000004 · NCATS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GRANDIS, JENNIFER RUBIN · 2012 to 2015
$78.0M
Maximizing Opportunities for Research Excellence - Evaluation Training SupplementR25GM056847 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DUNCAN, D'ANNE S., SELLO, JASON K · 1998 to 2023
$14.1M
UCSF Core Center for Musculoskeletal Biology and MedicineP30AR066262 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MAJUMDAR, SHARMILA · 2014 to 2018
$3.0M
Canonical Wnt Signaling as a Novel Regulator of Chondrocyte to Osteoblast Transdifferentiation during Endochondral Bone Repair in the MandibleF30DE026359 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WONG, SARAH ANNE · 2016 to 2021
$284k
NCATS NIH HHS UL1 TR000004NIAMS NIH HHS P30 AR066262NIDCR NIH HHS F30 DE026359NIGMS NIH HHS R25 GM056847
6 · The paper itself

Abstract

The majority of fractures heal through the process of endochondral ossification, in which a cartilage intermediate forms between the fractured bone ends and is gradually replaced with bone. Recent studies have provided genetic evidence demonstrating that a significant portion of callus chondrocytes transform into osteoblasts that derive the new bone. This evidence has opened a new field of research aimed at identifying the regulatory mechanisms that govern chondrocyte transformation in the hope of developing improved fracture therapies. In this article, we review known and candidate molecular pathways that may stimulate chondrocyte-to-osteoblast transformation during endochondral fracture repair. We also examine additional extrinsic factors that may play a role in modulating chondrocyte and osteoblast fate during fracture healing such as angiogenesis and mineralization of the extracellular matrix. Taken together the mechanisms reviewed here demonstrate the promising potential of using developmental engineering to design therapeutic approaches that activate endogenous healing pathways to stimulate fracture repair.

Indexed as

chondrocyte fatedevelopmental engineeringendochondral ossificationfracturetransdifferentiation

Identifiers

PMID29868574
PMCPMC5962790
OpenAlexW2808924447

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.