ArticleBurns & trauma2025
Fibroblast exosomes promote wound healing and improve the quality of healed skin via miR-29a-3p-mediated KEAP1/Nrf2 pathway activation.
Article in Burns & trauma, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Exosome and biotherapeutic strategies for dermatological and oncological skin complications.Annals of medicine · 2026Review
- Review
- The Tripartite Regulatory Framework of the Skin Extracellular Microenvironment and Related Anti-aging Strategies.Mini reviews in medicinal chemistry · 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
- Research progress on functionalized stem cell therapy strategies in wound healing.Frontiers in cell and developmental biology · 2026Review
- Role of Extracellular Vesicles in Skin Barrier Repair: Applications in Atopic Dermatitis and Chronic Wounds.International journal of nanomedicine · 2026Review
- Experimental study on tissue-engineered urethral graft for repairing urethral defects in a rabbit model.Frontiers in bioengineering and biotechnology · 2025Article
- Metabolism, senescence, and natural products: new perspectives on wound healing in diabetes.Frontiers in nutrition · 2025Review
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Authors and funding
14 authors.
Funding
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Abstract
Background: Wound healing is a sophisticated biological process characterized by the orchestrated interplay of diverse cellular components, growth factors, and signaling cascades. Recent research has highlighted the pivotal role of fibroblast exosomes in mediating intercellular communication and facilitating tissue regeneration. This investigation aimed to elucidate the therapeutic efficacy of fibroblast exosomes in enhancing wound repair mechanisms, with a particular emphasis on their differential effects in normal and diabetic wound healing paradigms. Methods: A mouse full-thickness skin defect model was used to evaluate the effects of fibroblast exosomes on wound re-epithelialization, granulation tissue formation, and epidermal barrier function. Molecular and cellular experiments were conducted to analyze the roles of exosomes in epidermal stem cell proliferation, migration, differentiation, and antioxidant stress, with further validation of the associated signaling pathways. The therapeutic efficacy was additionally confirmed in a type 1 diabetic mouse model. Results: Fibroblast exosomes significantly enhanced wound re-epithelialization by promoting the proliferation, migration, and differentiation of epidermal stem cells. Additionally, exosomes increased fibroblast abundance and myofibroblast activation, facilitating granulation tissue formation as well as improving extracellular matrix (ECM) deposition and the biomechanical properties of healed skin. Furthermore, exosomes improved epidermal barrier function by upregulating tight junction proteins (e.g. Claudin-1 and ZO-1) and reducing transepidermal water loss (TEWL). In diabetic mouse models, exosomes accelerated wound closure, restored ECM deposition and biomechanical integrity, and repaired epidermal barrier function. Mechanistically, exosomes target the 3' untranslated region (UTR) of Keap1 mRNA through miR-29a-3p and activate the KEAP1/Nrf2 antioxidant pathway, mitigating oxidative stress and protecting epidermal stem cells from reactive oxygen species (ROS)-induced damage. Conclusion: Fibroblast exosomes alleviate oxidative damage by modulating the KEAP1/Nrf2 pathway through miR-29a-3p and enhancing epidermal stem cell function. These exosomes exhibit remarkable therapeutic potential in accelerating wound healing and improving healing quality under both normal and diabetic conditions, offering a robust foundation for innovative therapeutic strategies.
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