Small extracellular vesicles derived from human adipose-derived stem cells regulate energetic metabolism through the activation of YAP/TAZ pathway facilitating angiogenesis.
Sun J., Lin Z., Liao Z., Wu Z., Li H., Wang H.
Laboratory Study, published in Cell Biol Int (2022) — 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
- Laboratory Study
- Journal
- Cell Biol Int (2022)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 36279478
- DOI
- 10.1002/cbin.11938
- Citations
- 3
Abstract (original English)
Recent studies have found small extracellular vesicles (sEVs) that are secreted from human adipose tissue-derived stem cells (hADSCs-sEVs) and contribute to angiogenesis. Glycolysis, the primary energetic pathway of vascular endothelial cells, plays a key role in the process of angiogenesis. However, hADSCs-sEVs' effects on energy metabolism within endothelial cells remain unclear. In our study, we found that hADSCs-sEVs restored glycolytic metabolism suppressed by 3-(pyridinyl)-1-(4-pyridinyl)-2-propen-1-one(3PO), a unique glycolytic inhibitor increasing the extracellular acidification rate (ECAR), oxygen consumption rate (OCR), glycolytic gene expression as well as pyruvate, lactate, and ATP production in HUVEC cells. In contrast, hADSCs-sEVs decreased PDH-E1α expression and acetyl-CoA production. The above results indicate that hADSCs-sEVs promote HUVEC angiogenesis via enhancing glycolysis and suppressing mitochondrial oxidative phosphorylation. Furthermore, we found that the YAP/TAZ pathway may play a key role in the effects hADSCs-sEVs have on HUVECs, thus, providing a promising approach for pro-angiogenesis-related regeneration.
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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