VAMP4 in hypoxic adipose stem cell exosomes alleviates ischemia-reperfusion injury.
Wang Y., Yu S., Wang X., Jin R., Liu F., Yang J.
Animal Study, published in Cell Mol Life Sci (2025) — summary generated from the PubMed abstract.
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
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
- Cell Mol Life Sci (2025)
- Country
- Switzerland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41460344
- PMCID
- PMC12748495
- DOI
- 10.1007/s00018-025-05967-4
Abstract (original English)
Background Ischemia/reperfusion injury (I/RI) impedes the progress of flap and allograft transplantation. Among various strategies to address oxidative stress (OS) and mitochondrial dysfunction associated with I/RI, exosomes derived from adipose-derived stem cells (ADSCs) subjected to hypoxia pretreatment show significant therapeutic potential. Methods and results This study assessed the effects of ADSC-derived exosomes (ADSC-Ex) from normoxic and hypoxic conditions on reactive oxygen species (ROS), mitochondrial calcium ion (Ca 2+ ) influx, mitochondrial potential, and cell apoptosis in an ischemia/reperfusion (I/R) model. Mass spectrometry (MS) was utilized to analyze differentially expressed proteins in hypoxic ADSC-Ex compared to normoxic controls. The functions of significantly upregulated proteins were investigated through knockdown experiments in hypoxic ADSC-Ex on alleviating I/R injury (I/RI) in HUVECs. Hypoxic ADSC-Ex significantly mitigated I/RI in vascular endothelial cells both in vitro and in vivo. This effect was associated with reduced ROS and mitochondrial Ca 2+ influx, and protection of mitochondrial potential. MS identified several proteins that were significantly upregulated in hypoxic ADSC-Ex, with Vesicle-associated membrane protein 4 (VAMP4) emerging as a pivotal molecule involved in alleviating I/RI in vascular endothelial cells. Conclusion This study de
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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