Evidence map›Paper›PMID 8941636›Full record

ArticleThe Journal of clinical investigation1996

Muscle differentiation during repair of myocardial necrosis in rats via gene transfer with MyoD.

C E Murry, M A Kay, T Bartosek, S D Hauschka, S M Schwartz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 144 citations in OpenAlex.

  1. Cardiac commitment driven by MyoD expression in pericardial stem cells.Frontiers in cell and developmental biology · 2024
    Article
  2. Genome Editing and Cardiac Regeneration.Advances in experimental medicine and biology · 2023
    Article
  3. Review
  4. Article
  5. Article
  6. Cardiac progenitor reprogramming for heart regeneration.Cell regeneration (London, England) · 2018
    Review
  7. Review
  8. Review
  9. Review
  10. Small mammalian animal models of heart disease.American journal of cardiovascular disease · 2016
    Review
  11. Review
  12. Heart regeneration, stem cells, and cytokines.Regenerative medicine research · 2014
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Heart regeneration.Nature · 2011
    Review
  18. Reprogramming fibroblasts into cardiomyocytes.The New England journal of medicine · 2011
    Article
  19. Review
  20. Angiomyogenesis for myocardial repair.Antioxidants & redox signaling · 2009
    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

5 authors at 1 institution in 1 country.

C E MurryDepartment of Pathology, University of Washington, Seattle 98195, USA. murry@u.washington.edu
M A Kay
T Bartosek
S D Hauschka
S M Schwartz
University of Washington · US

Funding

Striated Muscle Gene Transcription and Regulatory Gene Cassettes for Gene TherapyR01AR018860 · NIAMS · UNIVERSITY OF WASHINGTON · PI HAUSCHKA, STEPHEN DENISON · 1986 to 2012
$3.4M
REGULATION OF SKELETAL MUSCLE DIFFERENTIATIONR37AR018860 · NIAMS · UNIVERSITY OF WASHINGTON · PI HAUSCHKA, STEPHEN DENISON · 1993 to 2002
$1.0M
NHLBI NIH HHS HL-03174NHLBI NIH HHS HL-26404NIAMS NIH HHS AR-18860
6 · The paper itself

Abstract

Myocardial infarcts heal by scar formation because there are no stem cells in myocardium, and because adult myocytes cannot divide and repopulate the wound. We sought to redirect the heart to form skeletal muscle instead of scar by transferring the myogenic determination gene, MyoD, into cardiac granulation (wound repair) tissue. A replication-defective adenovirus was constructed containing MyoD under transcriptional control of the Rous sarcoma virus long terminal repeat. The virus converted cultured cardiac fibroblasts to skeletal muscle, indicated by expression of myogenin and skeletal myosin heavy chains (MHCs). To determine if MyoD could induce muscle differentiation in vivo, we injected 2 x 10(9) or 10(10) pfu of either the MyoD or a control beta-galactosidase adenovirus into healing rat hearts, injured 1 wk previously by freeze-thaw. After receiving the lower viral dose, cardiac granulation tissue expressed MyoD mRNA and protein, but did not express myogenin or skeletal MHC. When the higher dose of virus was administered, double immunostaining showed that cells in reparative tissue expressed both myogenin and embryonic skeletal MHC. No muscle differentiation occurred after beta-galactosidase transfection. Thus, MyoD gene transfer can induce skeletal muscle differentiation in healing heart lesions. Modifications of this strategy might eventually provide new contractile tissue to repair myocardial infarcts.

Indexed as

Genetic TherapyAdenoviridaeAnimalsbeta-GalactosidaseBlotting, NorthernCells, CulturedFibroblastsGene ExpressionGenetic EngineeringGenetic VectorsGene Transfer TechniquesImmunohistochemistryMaleMuscle, SkeletalMuscle, SmoothMyocardial Infarctionbeta-GalactosidaseMyoD ProteinMyogeninMyog protein, ratMyosin Heavy ChainsProteinsRNA, Messenger

Identifiers

PMID8941636
PMCPMC507669
OpenAlexW2133117273

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.