Evidence map›Paper›PMID 23336007›Full record

ArticlePloS one2013

Muscle side population cells from dystrophic or injured muscle adopt a fibro-adipogenic fate.

Christopher M Penton, Jennifer M Thomas-Ahner, Eric K Johnson, Cynthia McAllister, Federica Montanaro

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Intramuscular adipose tissue: from progenitor to pathology.American journal of physiology. Cell physiology · 2025
    Review
  3. Article
  4. MuSCs and IPCs: roles in skeletal muscle homeostasis, aging and injury.Cellular and molecular life sciences : CMLS · 2024
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Stem cell therapy for muscular dystrophies.The Journal of clinical investigation · 2020
    Review
  10. CD34 regulates the skeletal muscle response to hypoxia.Journal of muscle research and cell motility · 2019
    Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. 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

5 authors at 2 institutions in 1 country.

Christopher M PentonCenter for Gene Therapy, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, USA.
Jennifer M Thomas-Ahner
Eric K Johnson
Cynthia McAllister
Federica Montanaro
Nationwide Children's Hospital · USThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle side population (SP) cells are rare multipotent stem cells that can participate in myogenesis and muscle regeneration upon transplantation. While they have been primarily studied for the development of cell-based therapies for Duchenne muscular dystrophy, little is known regarding their non-muscle lineage choices or whether the dystrophic muscle environment affects their ability to repair muscle. Unfortunately, the study of muscle SP cells has been challenged by their low abundance and the absence of specific SP cell markers. To address these issues, we developed culture conditions for the propagation and spontaneous multi-lineage differentiation of muscle SP cells. Using this approach, we show that SP cells from wild type muscle robustly differentiate into satellite cells and form myotubes without requiring co-culture with myogenic cells. Furthermore, this myogenic activity is associated with SP cells negative for immune (CD45) and vascular (CD31) markers but positive for Pax7, Sca1, and the mesenchymal progenitor marker PDGFRα. Additionally, our studies revealed that SP cells isolated from dystrophic or cardiotoxin-injured muscle fail to undergo myogenesis. Instead, these SP cells rapidly expand giving rise to fibroblast and adipocyte progenitors (FAPs) and to their differentiated progeny, fibroblasts and adipocytes. Our findings indicate that muscle damage affects the lineage choices of muscle SP cells, promoting their differentiation along fibro-adipogenic lineages while inhibiting myogenesis. These results have implications for a possible role of muscle SP cells in fibrosis and fat deposition in muscular dystrophy. In addition, our studies provide a useful in vitro system to analyze SP cell biology in both normal and pathological conditions.

Indexed as

AdipogenesisCell DifferentiationAnimalsBiomarkersEndopeptidasesEndothelial CellsFemaleFibroblast Activation Protein AlphaFibroblastsFibrosisGelatinasesMembrane ProteinsMiceMuscle DevelopmentMusclesMuscular DystrophiesBiomarkersEndopeptidasesFibroblast Activation Protein AlphaGelatinasesMembrane ProteinsSerine Endopeptidases

Identifiers

PMID23336007
PMCPMC3545954
OpenAlexW2082639360

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.