ArticleCell biology and toxicology2025
GelMA hydrogel-loaded extracellular vesicles derived from keratinocytes promote skin microvasculature regeneration and wound healing in diabetic mice through activation of the PDGF-induced PI3K/AKT pathway.
Article in Cell biology and toxicology, 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.
- Harnessing the Therapeutic Potential of Extracellular Vesicles for Oral Wound Healing.Bioengineering (Basel, Switzerland) · 2026Review
- Induced membrane-mediated DBM in combination with PRP: an autologous bone graft substitute therapy with remarkable osteoformation potency for challenging bone defects.International journal of surgery (London, England) · 2026Article
- Role of Extracellular Vesicles in Skin Barrier Repair: Applications in Atopic Dermatitis and Chronic Wounds.International journal of nanomedicine · 2026Review
- Multidimensional Regulatory Mechanisms and Targeted Therapeutic Strategies for Inhibited Keratinocyte Proliferation in Diabetic Wounds.Drug design, development and therapy · 2026Review
- Extracellular Vesicle Therapies for Diabetic Skin Lesions: Mechanisms, Engineering, and Clinical Translation.International journal of nanomedicine · 2026Review
- From basic biology to engineered therapies: the keratinocyte stem cell playbook.Frontiers in medical technology · 2026Review
- Review
- Application of Biomaterials in Diabetic Wound Healing: The Recent Advances and Pathological Aspects.Pharmaceutics · 2025Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study explores how extracellular vesicles (EVs) derived from keratinocytes cultured in Gelatin Methacryloyl (GelMA) hydrogels facilitate microvascular regeneration and enhance wound repair in diabetic skin ulcers.
methodsEVs were harvested from keratinocyte cultures via ultracentrifugation and ultrafiltration, followed by characterization. Their uptake and angiogenic effects on human umbilical vein endothelial cells (HUVECs) were assessed in the following experimentations. Transcriptomic profiling of EV-treated HUVECs identified angiogenesis-related gene expression changes. A diabetic murine wound model was established and validated via glycemic profiling and pancreatic histology. In vivo effects of GelMA-EVs were evaluated through wound closure rates, histology (re-epithelialization, vascularization, collagen deposition), CD31 staining, and microvascular imaging.
resultsKeratinocyte-derived EVs significantly enhanced HUVEC proliferation, migration, and tube formation. Mechanistic studies reported elevated PDGF expression, activating the PI3K/AKT pathway. In vivo experiments validated that GelMA hydrogel-loaded EVs increased PDGF expression in wound tissues, promoting microvascular reconstruction and accelerating wound healing in diabetic mouse skin ulcers.
conclusionGelMA hydrogel-loaded EVs derived from keratinocytes upregulate PDGF, activating the PI3K/AKT pathway to promote microvascular network reconstruction and enhance wound healing in diabetic mouse skin ulcers.
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