Evidence map›Paper›PMID 24009313›Full record

ArticleHuman molecular genetics2014

Laminin-111 improves muscle repair in a mouse model of merosin-deficient congenital muscular dystrophy.

Pam M Van Ry, Priscilla Minogue, Bradley L Hodges, Dean J Burkin

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Micro-laminin gene therapy can function as an inhibitor of muscle disease in the dyMolecular therapy. Methods & clinical development · 2021
    Article
  9. Laminin-111 Improves the Anabolic Response to Mechanical Load in Aged Skeletal Muscle.The journals of gerontology. Series A, Biological sciences and medical sciences · 2021
    Article
  10. Article
  11. Article
  12. Review
  13. Zebrafish Models ofFrontiers in molecular neuroscience · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Treating pediatric neuromuscular disorders: The future is now.American journal of medical genetics. Part A · 2018
    Review
  20. 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

4 authors at 2 institutions in 1 country.

Pam M Van RyDepartment of Pharmacology, University of Nevada School of Medicine, Reno, NV 89557, USA and.
Priscilla Minogue
Bradley L Hodges
Dean J Burkin
University of Nevada, Reno · USProthelia (United States) · US

Funding

Outreach/Diversity/Pipeline ProjectP20GM103440 · NIGMS · UNIVERSITY OF NEVADA RENO · PI Eduardo A Robleto · 2012 to 2026
$58.0M
Integrin Alleviation of Muscular DystrophyR01AR053697 · NIAMS · UNIVERSITY OF NEVADA RENO · PI BURKIN, DEAN J. · 2008 to 2012
$1.2M
Intravenous Protein Therapy for Treatment of Congenital Muscular DystrophyR43AR057594 · NIAMS · PROTHELIA INC. · PI HODGES, BRADLEY L · 2009 to 2010
$237k
NIAMS NIH HHS R01AR053697NIAMS NIH HHS R43AR057594NIGMS NIH HHS 8 P20 GM103440
6 · The paper itself

Abstract

Merosin-deficient congenital muscular dystrophy type 1A (MDC1A) is a severe and fatal muscle-wasting disease with no cure. MDC1A patients and the dy(W-/-) mouse model exhibit severe muscle weakness, demyelinating neuropathy, failed muscle regeneration and premature death. We have recently shown that laminin-111, a form of laminin found in embryonic skeletal muscle, can substitute for the loss of laminin-211/221 and prevent muscle disease progression in the dy(W-/-) mouse model. What is unclear from these studies is whether laminin-111 can restore failed regeneration to laminin-α2-deficient muscle. To investigate the potential of laminin-111 protein therapy to improve muscle regeneration, laminin-111 or phosphate-buffered saline-treated laminin-α2-deficient muscle was damaged with cardiotoxin and muscle regeneration quantified. Our results show laminin-111 treatment promoted an increase in myofiber size and number, and an increased expression of α7β1 integrin, Pax7, myogenin and embryonic myosin heavy chain, indicating a restoration of the muscle regenerative program. Together, our results show laminin-111 restores muscle regeneration to laminin-α2-deficient muscle and further supports laminin-111 protein as a therapy for the treatment of MDC1A.

Indexed as

AnimalsFibrosisGene Expression RegulationLamininMiceMuscular AtrophyMuscular DystrophiesMuscular Dystrophy, AnimalMyogeninPAX7 Transcription FactorLamininMyogeninPax7 protein, mousePAX7 Transcription Factor

Identifiers

PMID24009313
PMCPMC3869356
OpenAlexW2166894867

What OpenQuestion holds

Textmetadata
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.