ArticleJournal of extracellular vesicles2025
Epidermal Stem Cell-Derived Extracellular Vesicles Induce Fibroblasts Mesenchymal-Epidermal Transition to Alleviate Hypertrophic Scar Formation via miR-200s Inhibition of ZEB1 and 2.
Article in Journal of extracellular vesicles, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Antifibrotic hydrogel strategies for scarless tissue regeneration: mechanisms, design, and application.Bioactive materials · 2027Review
- Epigenetic orchestration of scar formation: Therapeutic potential of targeting DNA methylation and non‑coding RNAs in cutaneous fibrosis (Review).Molecular medicine reports · 2026Review
- Cargo molecules in plasma neural-derived extracellular vesicles reveal pathological signatures of primary open-angle glaucoma.Journal of translational medicine · 2026Article
- The Role of MEF2 in Scar Formation and Angiogenesis.Journal of cosmetic dermatology · 2026Review
- Extracellular vesicle-mediated cell-cell communication in keloids and hypertrophic scars: mechanisms, methodological caveats, and therapeutic perspectives.Frontiers in cell and developmental biology · 2026Review
- Therapeutic value of mesenchymal stem cell-derived extracellular vesicles in hypertrophic and keloid scars: a systematic review and meta-analysis.Frontiers in cell and developmental biology · 2026Review
- Epidermal Stem Cell-Derived Extracellular Vesicles Induce Fibroblasts Mesenchymal-Epidermal Transition to Alleviate Hypertrophic Scar Formation via miR-200s Inhibition of ZEB1 and 2.Journal of extracellular vesicles · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Hypertrophic scar (HS) is a prevalent yet unresolved wound healing complication characterized by persistent hyperactive and proliferative fibroblasts, leading to excessive extracellular matrix (ECM) synthesis and collagen contraction. Our previous studies have identified epidermal stem cells (ESCs) as critical for wound healing and HS remodelling, with its extracellular vesicles (EVs) playing a vital role. However, the specific mechanisms remain unclear. In this study, we first discovered that ESC-EVs could effectively induce the mesenchymal-epidermal transition (MET) of HS fibroblasts (HSFs) and inhibit their biological activity. Furthermore, by next-generation sequencing and multiplexed CRISPR/Cas9 system, we elucidated that this therapeutic effect is mediated by the miR-200 family (miR-200s) encapsulated in ESC-EVs, which targeted and inhibited ZEB1 and ZEB2 in HSFs. This vital role and mechanism have been thoroughly validated in both in vitro cell experiments and in vivo rat tail HS (RHS) models. These findings not only shed light on a previously unidentified mechanism of ESC-EVs for HS, but also provide potential novel targets and strategies for its precise treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.