FGF-2-Overexpressing Adipose-Derived Stem Cells as a Paracrine Platform for Angiogenesis-Driven Tissue Regeneration.
Seki D., Honda M.
Laboratory Study, published in Cell Mol Bioeng (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Cell Mol Bioeng (2025)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41907095
- PMCID
- PMC13031578
- DOI
- 10.1007/s12195-025-00883-w
- Citations
- 1
Abstract (original English)
Background The survival and function of three-dimensional tissues critically depend on the establishment of a functional vascular network that ensures oxygen and nutrient supply and waste removal. Insufficient vascularization leads to hypoxia, metabolic stress, and cell death, making angiogenesis a fundamental requirement for successful tissue regeneration. This requirement is particularly evident in highly vascularized tissues such as bone, where vascular networks closely regulate tissue metabolism and repair. Methods Human adipose-derived mesenchymal stem cells (ASCs) were genetically modified to overexpress fibroblast growth factor 2 (FGF-2), a key regulator of angiogenesis. The angiogenic potential of these cells and the paracrine effects of their conditioned medium were subsequently evaluated, together with their effects on osteogenic differentiation to assess functional specificity. Results Overexpression of FGF-2 in ASCs enhanced endothelial cell migration and tube formation via paracrine mechanisms, in which elevated secretion of VEGFA and other angiogenic factors acted synergistically to promote angiogenesis. In contrast, osteogenic differentiation of ASCs was significantly inhibited by FGF-2 overexpression. Notably, FGFR2 expression, the receptor for FGF-2, was selectively downregulated during osteogenic induction, suggesting that sustained FGF-2 signaling preferentia
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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