Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMed

LLLT-ADSCs Curtail the Progression of Keloid Through Exosomal miR-26a-5p Downregulating Jag/Notch Pathway.

Han B., Yang J., Bai P., Jiao H., Yuan X., Shi J.

Laboratory Study on Scar, published in Lasers Surg Med (2026) — 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
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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
Lasers Surg Med (2026)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
42189761
DOI
10.1002/lsm.70135

Abstract (original English)

Background Adipose-derived stem cells treated with low-level laser light (LLLT-ADSCs) demonstrate an inhibitory effect on keloid scars, although the underlying molecular mechanisms remain largely unknown. This study aims to elucidate these mechanisms. Methods We investigated the morphology, quantity, and microRNA (miRNA) expression profiles of exosomes derived from LLLT-ADSCs compared to those from untreated ADSCs. Notably, hsa-miR-26a-5p was found to be highly expressed in exosomes from LLLT-ADSCs. We examined its impact on the proliferation, migration, and invasion of keloid fibroblasts (KFs) by modulating its expression levels in these cells. A dual-luciferase reporter assay was utilized to confirm the interaction between hsa-miR-26a-5p and the Jagged-1/Notch signaling pathway. Results Significant variations were observed in the exosomal contents between LLLT-ADSCs and ADSCs. Enhanced expression of hsa-miR-26a-5p was associated with reduced proliferation, migration, and invasion of KFs, along with diminished expression of Jagged-1 and NICD proteins. Conversely, suppression of hsa-miR-26a-5p expression reversed these effects. The dual-luciferase reporter system demonstrated that modifications in the binding sites of Jag-1 significantly mitigated the downregulation of Jag-1 expression induced by miRNA interaction. Conclusions LLLT-ADSCs can produce and deliver hsa-miR-26a-5p v

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
HumansMicroRNAsKeloidJagged-1 ProteinDown-RegulationSignal TransductionExosomesReceptors, NotchCell ProliferationCell Movement

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