Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

Adipose stem cells-derived microvesicles and chicken egg-derived exosomes attenuate cardiac ischemia/reperfusion injury through AKT/ERK/Nrf2/HO-1 axis to inhibit apoptosis and inflammation and restore autophagy.

Huang CM., Cheng YH., Lin YH., Chien CT.

Animal Study on Cardiovascular Disease, Chronic Inflammation, published in Life Sci (2026) — 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
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
Animal Study
Journal
Life Sci (2026)
Country
Netherlands
Reported sample size
—
Source database
PubMed
PMID
41921658
DOI
10.1016/j.lfs.2026.124364

Abstract (original English)

Aims Myocardial ischemia/reperfusion (I/R) injury is an unsolved medical issue that is caused by additional injuries derived from reperfusion therapy for patients with acute myocardial infarction, one of the leading causes of morbidity and mortality in the world. Myocardial I/R injury causes unpredictable complications evoked by oxidative stress, endothelial dysfunction, dysregulated autophagy, apoptosis, and an imbalanced inflammatory response. Microvesicles (MVs) derived from adipose stem cells (ADSC) and egg-derived exosomes (EXOs) may confer antioxidant, anti-inflammatory, anti-apoptotic and tissue repair potential, showing potential in cardiovascular therapy. This study aims to investigate the therapeutic effects and mechanisms of MVs and EXOs on myocardial I/R injury. Methods and materials To explore the underlying mechanisms, we examined the activation of the Akt and Erk signaling pathways, and analyzed the expression of endothelial nitric oxide synthase (eNOS), antioxidant proteins, autophagy, apoptotic related markers, and inflammatory cytokines. Key findings Peri-cardiac ischemic treatment of MVs or EXOs improved I/R depressed eNOS-mediated microcirculation, inhibited ST segment elevation, restored the elevated left ventricular end-diastolic pressure toward normal level, improved systolic and diastolic dysfunction (±dp/dt), reduced infarct size, decreased troponin I a

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
AnimalsApoptosisAutophagyMyocardial Reperfusion InjuryProto-Oncogene Proteins c-aktNF-E2-Related Factor 2ExosomesInflammationChickensMale

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