SVF
Level C· Early Human ResearchProspective Study

Charge-reversed small extracellular vesicles from human adipose-derived mesenchymal stromal cells attenuate renal fibrosis postacute kidney injury by inhibiting epithelial-mesenchymal transition progression in SD rat mod

Ping W., Xu X., Jiang Y., Yang R., Xu L.

Prospective Study on Chronic Kidney Disease, Acute Kidney Injury, published in Cytotherapy (2025) — summary generated from the PubMed abstract.

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
Prospective Study
Journal
Cytotherapy (2025)
Country
England
Reported sample size
—
PMID
40047734
DOI
10.1016/j.jcyt.2025.02.004

Abstract (original English)

Approximately 25% of patients with acute kidney injury (AKI) progress to chronic kidney disease, driven by the transition of renal tubular epithelial cells from epithelial to mesenchymal cells. Recent studies show that adipose-derived mesenchymal stromal cell-derived small extracellular vesicles (AMEV) can ameliorate renal fibrosis and injury. However, owing to poor retention, the limited bioavailability of AMEV hamper their therapeutic application. In this study, AMEV were extracted and modified with an ε-polylysine-polyethylene-distearoylphosphatidylethanolamine (PPD) polymer, which facilitated the reversal of the AMEV surface charge, thereby generating positively charged AMEV for the treatment of AKI. In a rat model of AKI, PPD modification significantly enhanced the renal retention of AMEV and effectively alleviated renal pathological damage. Further, RNA sequencing revealed that AMEV derived from adipose-derived mesenchymal stromal cells contains abundant microRNAs. We found that PPD modification significantly enhanced the bioavailability of AMEV and improved therapeutic effects in both in vivo and in vitro experiments. Furthermore, miR-100 enriched in AMEV targeted mTOR and suppressed the epithelial-mesenchymal transition phenotype of renal tubular epithelial cells, thereby alleviating renal fibrosis and promoting recovery of renal function postischemia-reperfusion. Overa

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Early human evidence such as case series or small samples, often without a control group.

How we grade evidence
AnimalsEpithelial-Mesenchymal TransitionMesenchymal Stem CellsExtracellular VesiclesHumansRatsFibrosisAcute Kidney InjuryDisease Models, AnimalRats, Sprague-Dawley
Face & SkinSystemic / IVChronic Kidney DiseaseAcute Kidney Injury
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