ArticleLasers in surgery and medicine2026
LLLT-ADSCs Curtail the Progression of Keloid Through Exosomal miR-26a-5p Downregulating Jag/Notch Pathway.
Article in Lasers in surgery and medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- LLLT-ADSCs Curtail the Progression of Keloid Through Exosomal miR-26a-5p Downregulating Jag/Notch Pathway.Lasers in surgery and medicine · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundAdipose-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.
methodsWe 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.
resultsSignificant 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.
conclusionsLLLT-ADSCs can produce and deliver hsa-miR-26a-5p via exosomes to suppress the Jagged-1/Notch pathway activation in KFs, thereby effectively preventing the progression of keloid scars. This mechanism presents a novel therapeutic strategy for managing keloid scars.
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