Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMed

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.

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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
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.

How we grade evidence
Epithelial-Mesenchymal TransitionAnimalsFibrosisExtracellular VesiclesForkhead Transcription FactorsMesenchymal Stem CellsHumansWnt Signaling PathwayMiceKidney

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