ArticleTissue engineering and regenerative medicine2026
Mesenchymal Stem Cell-Derived Extracellular Vesicles Attenuate Diabetic β-Cell Apoptosis and Dedifferentiation by Delivering miR-4436.
Article in Tissue engineering and regenerative medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundType 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by β-cell dysfunction and insulin resistance with limited treatment options. The targeting of pancreatic β-cell apoptosis and dedifferentiation represents a promising approach for T2DM therapy. Recently, mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have demonstrated repair potential for metabolic diseases. However, the effects of MSC-EVs on β-cell apoptosis and dedifferentiation in T2DM remain largely unclear.
methodsWe established db/db mouse model and high glucose-stimulated MIN6 cell model to evaluate the therapeutic efficacy of MSC-EVs in vivo and in vitro. Transcriptome sequencing, proteomic analysis, and microRNA (miRNA) sequencing were applied to explore the molecular mechanism underlying MSC-EV-induced β-cell protection.
resultsMSC-EVs significantly mitigated hyperglycemia, improved glucose tolerance, and restored β-cell function by preventing β-cell loss and reducing dedifferentiated β-cell populations in db/db mice. Mechanistically, MSC-EV treatment reversed hyperglycemia-induced ecotropic virus integration site 1 (EVI1) upregulation in β cells, and EVI1 knockdown significantly suppressed β-cell apoptosis and dedifferentiation by promoting forkhead box protein O1 (FOXO1) expression. MiRNA sequencing revealed that miR-4436 enriched in MSC-EVs inhibited EVI1 expression by directly binding to EVI1 mRNA. MiR-4436 knockdown abolished the therapeutic effects of MSC-EVs in T2DM
conclusionMSC-EVs inhibit pancreatic β-cell loss and dedifferentiation by miR-4436-mediated EVI1/FOXO1 regulation. Therefore, MSC-EV administration may represent a promising therapeutic strategy for T2DM.
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