Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

Cell-free extracts from human fat tissue attenuate ischemic injury in cardiomyocytes in a murine model

Yang TY., Sun Y., Zhang WJ., Wang CQ., Zhou J.

Animal Study on Cardiovascular Disease, published in World J Stem Cells (2025) — 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
World J Stem Cells (2025)
Reported sample size
—
Source database
Europe PMC
PMID
40503361
PMCID
PMC12149793
DOI
10.4252/wjsc.v17.i5.105394

Abstract (original English)

Background Ischemic heart disease ranks among the foremost contributors to mortality worldwide. Myocardial infarction injury poses a prevalent challenge in current therapies. Studies have shown that mesenchymal stem cell transplantation increases cytokine release, reduces myocardial cell necrosis, and improves left ventricular function; thus, it can be used to understand protective mechanisms. Fat extract (FE) derived from mesenchymal stem cell therapy contains high levels of paracrine factors. Aim To study the effects of FE on myocardial injury and its mechanism of action. Methods A mouse model of myocardial infarction and a hypoxic model of neonatal rat cardiomyocytes (CMs) were established to evaluate the effects of FE. Results FE exhibited an inhibitory effect on CM apoptosis and improved left ventricular function. This protective effect of FE on CMs was mediated, in part, by the activation of the phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin signaling pathway. Conclusion Our findings showed that FE could be a new treatment to protect CMs in ischemic heart disease.

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.

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