Evidence map›Paper›PMID 24898859›Full record

ArticleNature communications2014

Intramuscular adipogenesis is inhibited by myo-endothelial progenitors with functioning Bmpr1a signalling.

Ping Huang, Tim J Schulz, Ariane Beauvais, Yu-Hua Tseng, Emanuela Gussoni

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-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

30 citing papers in PubMed, 43 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Ping HuangDivision of Genetics, Boston Children's Hospital, Boston, Massachusetts 02115, USA.
Tim J Schulz1] Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Boston, Massachusetts 02115, USA [2].
Ariane Beauvais1] Division of Genetics, Boston Children's Hospital, Boston, Massachusetts 02115, USA [2].
Yu-Hua TsengSection on Integrative Physiology and Metabolism, Joslin Diabetes Center, Boston, Massachusetts 02115, USA.
Emanuela GussoniDivision of Genetics, Boston Children's Hospital, Boston, Massachusetts 02115, USA.
Boston Children's Hospital · USJoslin Diabetes Center · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Role of BMPs in Adipogenesis, Mitochondrial Function and Energy MetabolismR01DK077097 · NIDDK · JOSLIN DIABETES CENTER · PI TSENG, YU-HUA · 2007 to 2019
$5.6M
SP cells and downstream progenitors in human and mouse muscleR01NS047727 · NINDS · CHILDREN'S HOSPITAL BOSTON · PI GUSSONI, EMANUELA · 2004 to 2013
$2.9M
NICHD NIH HHS P30 HD018655NIDDK NIH HHS R01 DK077097NINDS NIH HHS NIH/NINDS2R01 NS047727NINDS NIH HHS R01 NS047727
6 · The paper itself

Abstract

Developing human muscle contains inter-myofibre progenitors expressing Bmp-receptor 1a (Bmpr1a) and Myf5 that respond to stimulation with Bmp4. Here we ablate Bmpr1a in Myf5- and MyoD-expressing cells in vivo. Mutant mice reveal increased intramuscular fat and reduced myofibre size in selected muscles, or following muscle injury. Myo-endothelial progenitors are the most affected cell type: clonal studies demonstrate that ablation of Bmpr1a in myo-endothelial cells results in decreased myogenic activity, while adipogenic differentiation is significantly increased. Downstream phospho-Smad 1, 5, 8 signalling is also severely decreased in mutant myo-endothelial cells. Lineage tracing of endothelial cells using VE-cadherin(Cre) driver failed to reveal a significant contribution of these cells to developing or injured skeletal muscle. Thus, myo-endothelial progenitors with functioning Bmpr1a signalling demonstrate myogenic potential, but their main function in vivo is to inhibit intramuscular adipogenesis, both through a cell-autonomous and a cell-cell interaction mechanism.

Indexed as

AdipogenesisAnimalsAntigens, CDBone Morphogenetic Protein Receptors, Type ICadherin 5CadherinsEndothelial CellsMiceMice, KnockoutMuscle, SkeletalMyoD ProteinMyogenic Regulatory Factor 5Signal TransductionSmad1 ProteinSmad5 ProteinSmad8 ProteinAntigens, CDBmpr1a protein, mouseBone Morphogenetic Protein Receptors, Type ICadherin 5CadherinsMyf5 protein, mouseMyoD1 myogenic differentiation proteinMyoD ProteinMyogenic Regulatory Factor 5Smad1 ProteinSmad1 protein, mouseSmad5 ProteinSmad5 protein, mouseSmad8 ProteinSmad9 protein, mouse

Identifiers

PMID24898859
PMCPMC4084855
OpenAlexW2073104176

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.