Evidence map›Paper›PMID 33248111›Full record

ArticleDevelopmental biology2021

Loss of Smad4 in the scleraxis cell lineage results in postnatal joint contracture.

Saundra Y Schlesinger, Seongkyung Seo, Brian A Pryce, Sara F Tufa, Douglas R Keene, Alice H Huang, Ronen Schweitzer

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Loss of the long form of Plod2 phenocopies contractures of Bruck syndrome-osteogenesis imperfecta.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
    Article
  6. Growth and mechanobiology of the tendon-bone enthesis.Seminars in cell & developmental biology · 2022
    Review
  7. SMAD4 contributes to chondrocyte and osteocyte development.Journal of cellular and molecular medicine · 2022
    Review
  8. Article
  9. 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

7 authors at 3 institutions in 1 country.

Saundra Y SchlesingerResearch Division, Shriners Hospital for Children, Portland, OR, 97239, USA.
Seongkyung SeoResearch Division, Shriners Hospital for Children, Portland, OR, 97239, USA.
Brian A PryceResearch Division, Shriners Hospital for Children, Portland, OR, 97239, USA.
Sara F TufaResearch Division, Shriners Hospital for Children, Portland, OR, 97239, USA.
Douglas R KeeneResearch Division, Shriners Hospital for Children, Portland, OR, 97239, USA.
Alice H HuangDepartment of Orthopedic, Icahn School of Medicine at Mount Sinai, New York, NY, 10037, USA.
Ronen SchweitzerResearch Division, Shriners Hospital for Children, Portland, OR, 97239, USA; Department of Orthopedics, Oregon Health and Science University, Portland, OR, USA. Electronic address: schweitz@ohsu.edu.
Shriners Hospitals for Children - Portland · USIcahn School of Medicine at Mount Sinai · USOregon Health & Science University · US

Funding

Experimental Resources for Studies of Tenocyte Differentiation and Cell Fate DiversityR01AR072716 · NIAMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI SCHWEITZER, RONEN · 2018 to 2022
$1.7M
Transcriptional regulation of tendon differentiation and matrix formationR01AR055973 · NIAMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI SCHWEITZER, RONEN · 2010 to 2014
$1.7M
REGULATION OF TENDON INDUCTION AND FORMATION BY TGFbeta SIGNALINGR01AR055640 · NIAMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI SCHWEITZER, RONEN · 2007 to 2011
$1.6M
Maintenance and Regulation of Tendon and Ligament Maturation by TGFbeta SignalingR01AR067211 · NIAMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI SCHWEITZER, RONEN · 2016 to 2020
$1.5M
NIAMS NIH HHS R01 AR055640NIAMS NIH HHS R01 AR055973NIAMS NIH HHS R01 AR067211NIAMS NIH HHS R01 AR072716
6 · The paper itself

Abstract

Growth of the musculoskeletal system requires precise coordination between bone, muscle, and tendon during development. Insufficient elongation of the muscle-tendon unit relative to bone growth results in joint contracture, a condition characterized by reduction or complete loss of joint range of motion. Here we establish a novel murine model of joint contracture by targeting Smad4 for deletion in the tendon cell lineage using Scleraxis-Cre (ScxCre). Smad4

Indexed as

AnimalsBone DevelopmentBone Morphogenetic ProteinsCartilageCell LineageCollagenContractureExtracellular MatrixForelimbMiceMuscle, SkeletalSignal TransductionSmad4 ProteinTendonsTransforming Growth Factor betaBone Morphogenetic ProteinsCollagenSmad4 ProteinSmad4 protein, mouseTransforming Growth Factor betaBMPJoint contractureSmad4TendonTGFβ

Identifiers

PMID33248111
PMCPMC9105544
OpenAlexW3108010375

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.