Evidence map›Paper›PMID 30282911›Full record

ArticleMetabolites2018

Metabolomic Analyses Reveal Extensive Progenitor Cell Deficiencies in a Mouse Model of Duchenne Muscular Dystrophy.

Josiane Joseph, Dong Seong Cho, Jason D Doles

Open access · goldAbstract read
In one paragraph

Article in Metabolites, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Caveolin and NOS in the Development of Muscular Dystrophy.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
  6. A TGF-β/KLF10 signaling axis regulates atrophy-associated genes to induce muscle wasting in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Article
  8. Review
  9. Biomarkers in Duchenne Muscular Dystrophy.Current heart failure reports · 2022
    Review
  10. Article
  11. Review
  12. Complementary NADSkeletal muscle · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. A comparison of the bone and growth phenotype ofDisease models & mechanisms · 2020
    Article
  17. Article
  18. Article
  19. Review
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

3 authors at 1 institution in 1 country.

Josiane JosephDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA. joseph.josiane@mayo.edu.ORCID 0000-0002-2009-9373
Dong Seong ChoDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA. cho.dong@mayo.edu.
Jason D DolesDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA. Doles.Jason@mayo.edu.ORCID 0000-0002-6830-708X
Mayo Clinic · US

Funding

TRAINING IN TRANSLATIONAL RESEARCH: BENCH TO BEDSIDER25GM055252 · NIGMS · MAYO CLINIC ROCHESTER · PI LUJAN, LUIS, MAHER, LOUIS JAMES · 1996 to 2022
$8.3M
Medical Scientist Traning Program at Mayo ClinicT32GM065841 · NIGMS · MAYO CLINIC ROCHESTER · PI KAUFMANN, SCOTT H, SCHIMMENTI, LISA A · 2003 to 2022
$5.8M
Post-transcriptional Regulation of Satellite Cell FunctionR00AR066696 · NIAMS · MAYO CLINIC ROCHESTER · PI DOLES, JASON · 2016 to 2018
$961k
National Institutes of Health AR66696NIAMS NIH HHS R00 AR066696NIGMS NIH HHS R25 GM055252NIGMS NIH HHS T32 GM065841
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a musculoskeletal disorder that causes severe morbidity and reduced lifespan. Individuals with DMD have an X-linked mutation that impairs their ability to produce functional dystrophin protein in muscle. No cure exists for this disease and the few therapies that are available do not dramatically delay disease progression. Thus, there is a need to better understand the mechanisms underlying DMD which may ultimately lead to improved treatment options. The muscular dystrophy (MDX) mouse model is frequently used to explore DMD disease traits. Though some studies of metabolism in dystrophic mice exist, few have characterized metabolic profiles of supporting cells in the diseased environment. Using nontargeted metabolomics we characterized metabolic alterations in muscle satellite cells (SCs) and serum of MDX mice. Additionally, live-cell imaging revealed MDX-derived adipose progenitor cell (APC) defects. Finally, metabolomic studies revealed a striking elevation of acylcarnitines in MDX APCs, which we show can inhibit APC proliferation. Together, these studies highlight widespread metabolic alterations in multiple progenitor cell types and serum from MDX mice and implicate dystrophy-associated metabolite imbalances in APCs as a potential contributor to adipose tissue disequilibrium in DMD.

Indexed as

adipose tissueDuchenne muscular dystrophymetabolomicsskeletal musclestem cells

Identifiers

PMID30282911
PMCPMC6315702
OpenAlexW2894742196

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.