Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMed

Human adipose tissue-derived stem cells protect impaired cardiomyocytes from hypoxia/reoxygenation injury through hypoxia-induced paracrine mechanism.

Yang J., Zhang H., Zhao L., Chen Y., Liu H., Zhang T.

Laboratory Study on Cardiovascular Disease, published in Cell Biochem Funct (2012) — summary generated from the PubMed abstract.

Open my reading list
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
Read the A–D evidence level guide

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
Laboratory Study
Journal
Cell Biochem Funct (2012)
Country
England
Reported sample size
—
Source database
PubMed
PMID
22610511
DOI
10.1002/cbf.2829
Citations
23

Abstract (original English)

Growing studies have emerged on adipose-derived stem cells (ADSCs), which hold the potential for cell-based therapy in diseased injured hearts. Apart from their differentiation pluripotency, such benefits also result from the ability of paracrine. The results of this study showed that after a 24-h hypoxia culture, ADSCs secreted amplified quantities of hepatocyte growth factor, interleukin-1, vascular endothelial growth factor-A, fibroblast growth factor-2, and transforming growth factor-β, all of which increased statistically compared with normoxia cultures. Resultantly, conditioned media (CM) from hypoxia-treated ADSCs can promptly improve cardiac function in in vivo infarction model as well as ameliorate apoptosis of cardiomyocytes subjected to hypoxia/reoxygenation conditions, accompanied by changes of JNK signal activation. While SP600125, a specific JNK pathway inhibitor, partly decreased cardiac cytoprotection assessed by incremental caspase-3 activation and subsequent TUNEL index, which led to no significantly different outcome between CM from ADSCs in normoxia culture and those in hypoxia culture. These data suggested that, in response to hypoxia, ADSCs could amplify expression of several protective soluble factors, which mediate direct cytoprotection. Furthermore, the improvement for impaired cardiomyocytes treated by hypoxia-induced ADSCs-CM was significant in part b

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
Adipose TissueAnthracenesCell HypoxiaCells, CulturedCytoprotectionHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMyocytes, CardiacOxygen

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.

Related research