ArticleStem cell research & therapy2025
Extracellular vesicle-derived lncRNA VIM-AS1 promotes diabetic wound healing by promoting glycolysis and alleviating cellular senescence.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Exosomal lncRNAs in Cerebrovascular Diseases: Biomarkers, Pathological Mechanisms, and Therapeutic Potential.Non-coding RNA · 2026Review
- Comparative transcriptome analysis of Qinchuan and Wagyu cattle reveals lnc11599 as a negative regulator of intramuscular fat deposition.BMC genomics · 2026Article
- Charting the expression landscape of human long non-coding RNAs across diverse biological contexts with LncExpDB 2.0.Nucleic acids research · 2026Article
- Dual modes of action: direct regulation and ceRNA-mediated mechanisms of ncRNAs in dermal fibroblast senescence.Frontiers in cell and developmental biology · 2026Review
- Investigating the Mechanistic Link Between Lactate-Induced Histone Lactylation and Cellular Senescence in Osteoarthritis Chondrocytes: Implications for Therapy.International journal of biological sciences · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
aimsDiabetic wound healing is a significant challenge due to impaired cellular functions, and current therapeutic approaches often prove inadequate. This study aims to explore the role of extracellular vesicles (EVs) derived from human umbilical mesenchymal stem cells (HuMSCs), particularly focusing on their associated long non-coding RNAs (lncRNAs), in promoting diabetic wound repair.
methodsTo investigate this, we employed lncRNA sequencing of EVs, created reprogrammed EVs, and utilized a diabetic rat model. The impact of HuMSCs-derived EVs on fibroblast glycolysis, proliferation, and migration was assessed, along with the function of lncRNA VIM-AS1 in glucose metabolism via the PPAR-γ pathway.
resultsOur results demonstrate that HuMSCs-derived EVs enhance glycolysis in fibroblasts, which is essential for effective wound healing. We identified lncRNA VIM-AS1 as a pivotal regulator that not only promotes fibroblast proliferation and migration but also significantly enhances endothelial cell function, specifically regarding angiogenesis and tissue vascularization. Furthermore, EVs-derived lncRNA VIM-AS1 was found to reduce reactive oxygen species (ROS) levels, thereby mitigating oxidative stress and cellular senescence in both fibroblasts and endothelial cells. In vivo experiments in rat models confirmed the capacity of EVs-derived lncRNA VIM-AS1 to improve diabetic wound healing.
conclusionsThis study highlights the therapeutic potential of HuMSCs-derived EVs and specifically lncRNA VIM-AS1 as innovative approaches to address the challenges of tissue repair in diabetic conditions, offering promising strategies for enhancing wound healing efficacy.
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