ArticleDiabetologia2025
bFGF rescues dysfunctional properties of adipose-derived stem cells from individuals with type 2 diabetes by modulating their miRNA profile.
Article in Diabetologia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Type 2 Diabetes-Induced Molecular and Functional Impairment of Adipose Tissue-Derived Mesenchymal Stromal Cells (ASCs) and Interferon Gamma Priming for Enhanced Diabetic ASC-Based Therapy.Stem cell reviews and reports · 2026Article
- Review
- Adipose Tissue Engineering Biomaterials: Smart Scaffolds, Vascularization, and Clinical Frontiers.Biomolecules · 2026Review
- Obesity Alters the microRNA Expression Profile Related to Metabolic Disorders in Peripheral Blood Mononuclear Cells: Preliminary Results.Current issues in molecular biology · 2025Article
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Authors and funding
7 authors.
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Abstract
aims/hypothesisThe aim of this study was to investigate whether basic fibroblast growth factor (bFGF) can restore the proliferation and migration capacities of adipose-derived stem cells (ASCs), which are impaired by type 2 diabetes, and improve vascular remodelling.
methodsASCs obtained from individuals with or without diabetes were cultured with 10 ng/ml bFGF for 9 days. The ASCs were phenotypically characterised and functionally tested for proliferation capacity. Differentially expressed miRNAs before and after treatment were analysed using miRNA arrays. Crosstalk between ASCs and human vascular smooth muscle cells (HVSMCs) was assessed using wound healing, transwell migration and co-culture assays. Finally, a Matrigel plug assay in nude mice was used to evaluate the contribution of ASCs to neovessel formation.
resultsbFGF treatment significantly enhanced the proliferation and migration of ASCs from individuals with type 2 diabetes (T2DM ASCs), and altered the expression of miRNAs associated with ASC proliferation. ASCs promoted HVSMC migration and, when co-cultured, facilitated tube-like structure formation. In vivo Matrigel plug assays revealed that bFGF treatment enhanced neovessel formation. Although both non-T2DM ASCs (ASCs from individuals without type 2 diabetes) and untreated T2DM ASCs stimulated angiogenesis, bFGF-treated subcutaneous and visceral T2DM ASCs promoted even greater neovessel formation. Additionally, bFGF treatment modulated the expression of multiple angiogenesis-related miRNAs in ASCs. CONCLUSIONS/
interpretationPreconditioning T2DM ASCs with bFGF alters their miRNA profile, enhancing cell proliferation and their vascular remodelling potential. This strategy could improve the therapeutic utility of T2DM ASCs.
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