Exosomes Derived from ADSCs Attenuate Sepsis-Induced Lung Injury by Delivery of Circ-Fryl and Regulation of the miR-490-3p/SIRT3 Pathway.
Shen W., Zhao X., Li S.
Animal Study, published in Inflammation (2021) — 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
- Inflammation (2021)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 34478012
- DOI
- 10.1007/s10753-021-01548-2
- Citations
- 48
Abstract (original English)
Sepsis-induced lung injury is a clinical syndrome characterized by injury of alveolar epithelium cells (AECs). Previous investigations illustrate that exosomes secreted from adipose-derived stem cells (ADSCs) have therapeutic effects in a variety of disease treatments, but roles and mechanisms regarding ADSC-derived exosomes in sepsis-induced lung injury are unclear. In this study, high-throughput sequencing was used to explore the molecular delivery of ADSC exosomes. A sepsis-induced lung injury mouse model and a lipopolysaccharide-induced AEC damage model were used for mechanistic analysis. The results showed that ADSC exosomes have high levels of the circular RNA (circ)-Fryl. Downregulation of circ-Fryl suppressed ADSC protective effects exosomes against sepsis-induced lung injury by decreasing apoptosis and inflammatory factor expression. Bioinformatics and luciferase reporting experiments showed that miR-490-3p and SIRT3 are downstream targets of circ-Fryl. miR-490-3p overexpression or SIRT3 silencing reversed ADSC exosome protective effects. Studying the mechanism showed that overexpression of circ-Fryl promoted autophagy activation by inducing SIRT3/AMPK signaling. Autophagy activation can suppress sepsis-induced lung injury by decreasing apoptosis and inflammatory factor expression. Taken together, our results suggest that exosomes derived from ADSCs attenuate sepsis-in
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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