Evidence map›Paper›PMID 40256763›Full record

ArticleJBMR plus2025

Alpha-smooth muscle actin-expressing dermal sheath cells are a major cellular contributor to heterotopic subcutaneous ossifications in a mouse model of Albright hereditary osteodystrophy.

Patrick McMullan, Peter Maye, Sierra H Root, Qingfen Yang, Sarah Edie, David Rowe, Ivo Kalajzic, Emily L Germain-Lee

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JBMR plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Patrick McMullanDepartment of Pediatrics, University of Connecticut School of Medicine, Farmington, CT 06030, United States.
Peter MayeDepartment of Reconstructive Sciences, Center for Regenerative Medicine and Skeletal Development, University of Connecticut School of Dental Medicine, Farmington, CT 06030, United States.
Sierra H RootDepartment of Reconstructive Sciences, Center for Regenerative Medicine and Skeletal Development, University of Connecticut School of Dental Medicine, Farmington, CT 06030, United States.
Qingfen YangDepartment of Pediatrics, University of Connecticut School of Medicine, Farmington, CT 06030, United States.
Sarah EdieThe Jackson Laboratory, Farmington, CT 06032, United States.
David RoweDepartment of Reconstructive Sciences, Center for Regenerative Medicine and Skeletal Development, University of Connecticut School of Dental Medicine, Farmington, CT 06030, United States.
Ivo KalajzicDepartment of Reconstructive Sciences, Center for Regenerative Medicine and Skeletal Development, University of Connecticut School of Dental Medicine, Farmington, CT 06030, United States.
Emily L Germain-LeeDepartment of Pediatrics, University of Connecticut School of Medicine, Farmington, CT 06030, United States.ORCID https://orcid.org/0000-0002-5727-610X

Funding

Skeletal, Craniofacial and Oral Biology Training GrantT90DE021989 · NIDCR · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MINA, MINA · 2011 to 2022
$4.5M
Skeletal Phenotyping of Heterozygotes from IMPC Embryonic Lethal LinesR01HD098636 · NICHD · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MAYE, PETER, ROWE, DAVID W. · 2019 to 2023
$2.8M
The role of G protein-coupled signaling in neurocognitive and psychosocialabnormalitiesR21HD078864 · NICHD · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI GERMAIN-LEE, EMILY L · 2016 to 2017
$451k
NICHD NIH HHS R01 HD098636NICHD NIH HHS R21 HD078864NIDCR NIH HHS T90 DE021989
6 · The paper itself

Abstract

Heterotopic ossifications (HOs) are the pathologic process by which bone inappropriately forms outside of the skeletal system. Despite HOs being a persistent clinical problem in the general population, there are no definitive strategies for their prevention and treatment due to a limited understanding of the cellular and molecular mechanisms contributing to lesion development. One disease in which the development of heterotopic subcutaneous ossifications (SCOs) leads to morbidity is Albright hereditary osteodystrophy (AHO). Albright hereditary osteodystrophy is caused by heterozygous inactivation of

Indexed as

Albright hereditary osteodystrophydermal sheathGNAShair follicleheterotopic ossificationpseudohypoparathyroidismpseudopseudohypoparathyroidismsecreted frizzled related protein 2SFRP2subcutaneous ossification

Identifiers

PMID40256763
PMCPMC12009542

What OpenQuestion holds

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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.