ArticleScientific reports2025
Retarding human adipose-derived MSCs senescence and promoting tendon repair using cell sheet engineering with a histone methyltransferase inhibitor.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Immune-epigenetic convergence in biomaterial-guided tissue regeneration.Materials today. Bio · 2026Article
- Mesenchymal stem/stromal cell senescence in aging and regenerative medicine: a systematic review.Biogerontology · 2026Review
- Advanced bioactive materials and strategies for tendon repair and function restoration.Journal of orthopaedic translation · 2025Review
- Biological tendon regeneration, are we almost there or is it still a stretch?Regenerative medicine · 2025Article
- SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.Journal of inflammation research · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Mesenchymal stem cell (MSC) holds immense potential as candidates for cell therapy in the treatment of tendon injuries due to their remarkable ability for multiple cell differentiation. However, the proliferative and differentiation capacity of MSCs has been limited by cellular senescence during the process of expanding culture. Therefore, in this study, our aim was to maintain the beneficial properties of MSCs. We found that SETD7, a histone methyltransferase, was upregulated during ex vivo expansion of human adipose-derived mesenchymal stem cells (hAD-MSCs). Pharmacological inhibition of SETD7 with PFI-2 in hAD-MSCs cultures delayed their senescence, as evident by the diminished expression of senescent-associated genes and the maintenance of their proliferation and differentiation capacity. Upon transplantation, cell sheets derived from hAD-MSCs expanded with PFI-2 were better able to accelerate tendon repair. Therefore, the present findings reveal that SETD7 is an important target to improve the expansion of hAD-MSCs by delaying senescence, which is importance for the development of efficient stem cell-based therapeutic approaches.
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