Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Reconstitute the damaged heart via the dual reparative roles of pericardial adipose-derived flk-1+ stem cells.

Wang X., Liu X., Zhang H., Nie L., Chen M., Ding Z.

Animal Study on Cardiovascular Disease, published in Int J Cardiol (2015) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Int J Cardiol (2015)
Country
Netherlands
Reported sample size
—
Source database
PubMed
PMID
26407047
DOI
10.1016/j.ijcard.2015.09.002
Citations
9

Abstract (original English)

The pericardial adipose derived stromal cells (pADSC) own a developmental origin from the "second heart field" and thus favor myogenic differentiation. The present experiments extended our previous observation by defining a subset of pADSC marked with the expression of flk-1, a type II receptor for VEGF to efficiently enhance cardiac repair. Immunofluorescence and flow cytometry showed that flk-1 positive cells represented about 12% in the pericardial tissue and the total isolated pADSC. The purified flk-1 positive pADSC by magnetic sorting (flk-1pospADSC) show the ability of forming spherical structure in which both myogenic (cTnT+) and angiogenic (vWF+) precursors were concurrently generated in culture. After being intramyocardially transplanted into the ischemic hearts, flk-1pospADSC yielded superior structural repair to PBS control or flk-1negpADSC, characterized by the thickening of the infarcted wall in which both myogenesis and angiogenesis of microvasculature (preferentially with ϕ<50 μm) were significantly ensured (p<0.01). The structure benefits were also translated into a functional restoration 28 days after transplantation (EF=44% vs. 62%, p<0.01). Further pulse-chase labeling experiments with BrdU revealed that neomyogenesis and neoangiogenesis contribute in the structural repair. The newly formed myocardium was resulted from the proliferation of pre-existing cardi

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AdipocytesAnimalsCell DifferentiationCells, CulturedDisease Models, AnimalFlow CytometryImmunohistochemistryMaleMyocardial InfarctionPericardium

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