Adipose mesenchymal stem cell-derived extracellular vesicles alleviate renal fibrosis by reducing epithelial-mesenchymal transition via the FOXS1/Wnt/β-catenin signaling pathway.
Sun J., Jia Y., Chen S., Bian Y., Liang H., Du X.
Animal Study on Chronic Kidney Disease, published in Int Immunopharmacol (2024) — 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
- Int Immunopharmacol (2024)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 39709913
- DOI
- 10.1016/j.intimp.2024.113880
Abstract (original English)
Adipose mesenchymal stem cells (ADSCs) exert beneficial effects on kidney disease through a paracrine mechanism. However, the specific molecular mechanisms by which ADSCs treat renal fibrosis are not yet fully understood. Therefore, it is crucial to clarify the therapeutic effects of ADSC-derived extracellular vesicles (ADSC-EVs) on the progression of renal fibrosis and their underlying mechanisms. We investigated the therapeutic effects of ADSC-EVs on renal fibrosis both in vivo and in vitro. Key genes and signaling pathways were identified with RNA sequencing analysis of HK-2 cells. The role and underlying mechanism of the FOXS1/Wnt/β-catenin pathway in mediating antifibrotic effects were also verified. In vivo, We found that ADSC-EV treatment significantly improves renal fibrosis in unilateral ureteral obstruction (UUO)-induced renal fibrosis mice models. And in vitro, our data suggested that ADSC-EVs can reduce epithelial-mesenchymal transition (EMT) to inhibit fibrosis in transforming growth factor-β1 (TGF-β1)-treated HK-2 cells. The RNA sequencing results showed that FOXS1 was the primary gene involved in ADSC-EV treatment of renal fibrosis. RT-qPCR suggested that ADSC-EV treatment reversed elevated FOXS1 level both in TGF-β1-treated HK-2 cells and UUO-induced renal fibrosis mice models. Moreover, Western blot analysis confirmed that ADSC-EVs alleviate renal fibrosis and
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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