Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Adipose Mesenchymal Stem Cell Exosomes Regulate Ferroptosis via ATF3 to Attenuate Acute Myocardial Infarction.

Chen L., Liu Z., Wang L., Gu M., Luo Y.

Animal Study on Cardiovascular Disease, published in Ann Clin Lab Sci (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
Ann Clin Lab Sci (2025)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
40089274

Abstract (original English)

During acute myocardial infarction (AMI), ferroptosis occurs in cardiomyocytes, leading to ventricular remodeling. To investigate the influence of exosomes (Exo) derived from adipose mesenchymal stem cells (AD-MSCs) on cardiomyocytes, a therapeutic approach to resolve AMI may be discovered. The Exo of AD-MSCs was isolated and identified, and internalized into cardiomyocytes. In vitro , oxygen-sugar deprivation (OGD) was performed to cultivate H9C2 cells to simulate the AMI model, and H9C2 cells incubated with Exo. In addition, an AMI rat model was constructed, and Exo was injected into the edge of myocardial infarction. The levels of MDA, Fe 2+ , GSH, and GPX4 were detected using corresponding kit, the expression levels of ATF3, SLC7A11, PTGS2, and GPX4 were detected using western blot. The oe-ATF3 plasmid was transfected into H9C2 cells to explore the mechanism of ferroptosis regulation by Exo. Exo was isolated and identified successfully, and further confirmed that it could be internalized into H9C2 cells. Compared with the control group, the level of apoptosis and ferroptosis in OGD group was significantly increased, while the level of cell vitality was significantly decreased. After Exo treatment, the level of ferroptosis and apoptosis was significantly decreased, while the level of cell vitality was significantly increased. However, after overexpression of ATF3 in cells, i

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
FerroptosisAnimalsExosomesMesenchymal Stem CellsMyocardial InfarctionActivating Transcription Factor 3RatsMyocytes, CardiacMaleRats, Sprague-Dawley

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