Evidence map›Paper›PMID 24460869›Full record

ArticleStem cell research & therapy2014

Extracellular matrix remodeling following myocardial infarction influences the therapeutic potential of mesenchymal stem cells.

Kelly Elizabeth Sullivan, Kyle Patrick Quinn, Katherine Michele Tang, Irene Georgakoudi, Lauren Deems Black

Abstract read
In one paragraph

Article in Stem cell research & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
–field-weighted citation impact
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

61 citing papers in PubMed.

  1. Article
  2. Review
  3. Biocompatibility of decellularized spinach leaves.npj biomedical innovations · 2025
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  12. Biomimetic design of bioartificial scaffolds for theFrontiers in bioengineering and biotechnology · 2022
    Article
  13. Article
  14. Towards organoid culture without Matrigel.Communications biology · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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.

Kelly Elizabeth Sullivan
Kyle Patrick Quinn
Katherine Michele Tang
Irene Georgakoudi
Lauren Deems Black

Funding

Restoring LV Function Post-MI Using Fibrin-Gel Based Engineered MyocardiumR00HL093358 · NHLBI · TUFTS UNIVERSITY MEDFORD · PI BLACK III, LAUREN D. · 2010 to 2012
$747k
NHLBI NIH HHS R00HL093358
6 · The paper itself

Abstract

introductionAlthough stem cell therapy is a promising treatment for myocardial infarction, the minimal functional improvements observed clinically limit its widespread application. A need exists to maximize the therapeutic potential of these stem cells by first understanding what factors within the infarct microenvironment affect their ability to regenerate the necrotic tissue. In this study, we assessed both differentiation capacity and paracrine signaling as a function of extracellular matrix remodeling after myocardial infarction.

methodsMechanical and compositional changes to the decellularized infarcted myocardium were characterized to understand how the extracellular environment, specifically, was altered as a function of time after coronary artery ligation in Sprague-Dawley rats. These alterations were first modeled in a polyacrylamide gel system to understand how the variables of composition and stiffness drive mesenchymal stem cell differentiation towards a cardiac lineage. Finally, the paracrine secretome was characterized as a function of matrix remodeling through gene and protein expression and conditioned media studies.

resultsThe decellularized infarct tissue revealed significant alterations in both the mechanical and compositional properties of the ECM with remodeling following infarction. This altered microenvironment dynamically regulates the potential for early cardiac differentiation. Whereas Nkx2.5 expression is limited in the presence of chronic remodeled matrix of increased stiffness, GATA4 expression is enhanced. In addition, the remodeled matrix promotes the expression of several proangiogenic, prosurvival, antifibrotic, and immunomodulatory growth factors. In particular, an increase in HGF and SDF1 expression and secretion by mesenchymal stem cells can rescue oxidatively stressed cardiomyocytes in vitro.

conclusionsThis study demonstrated that decellularization of diseased tissue allows for the exclusive analysis of the remodeled matrix and its ability to influence significantly the cellular phenotype. Characterization of cell fate as a function of myocardial remodeling following infarction is critical in developing the ideal strategy for cell implantation to maximize tissue regeneration and to ultimately reduce the prevalence and severity of heart failure.

Indexed as

Mesenchymal Stem Cell TransplantationAnimalsCell DifferentiationCells, CulturedChemokine CXCL12Extracellular MatrixGATA4 Transcription FactorHepatocyte Growth FactorHomeobox Protein Nkx-2.5Homeodomain ProteinsMaleMesenchymal Stem CellsMyocardial InfarctionMyocytes, CardiacParacrine CommunicationRatsChemokine CXCL12Gata4 protein, ratGATA4 Transcription FactorHepatocyte Growth FactorHomeobox Protein Nkx-2.5Homeodomain ProteinsNkx2-5 protein, ratTranscription Factors

Identifiers

PMID24460869
PMCPMC4055039

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Registered trials

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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.