Chondrogenic potential of mesenchymal progenitors from somatic and cartilage-derived iPSCs is predicted by their transcriptomic signatures.
Khan NM., Doan TN., Kaiser JM., Drissi H.
Laboratory Study on Cartilage Damage, published in Genes Dis (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
- Genes Dis (2025)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41492477
- PMCID
- PMC12765249
- DOI
- 10.1016/j.gendis.2025.101730
Abstract (original English)
Mesenchymal stem cells (MSCs) are widely used in regenerative therapy but face limitations like low abundance, replicative senescence, donor variability, and restricted plasticity. Induced pluripotent stem cell-derived MSCs (iMSCs) may provide an alternative, but their similarities or intrinsic differences with adult MSCs remain unknown. This study compares the chondrogenic potential of iMSCs derived from chondrocyte-specific induced pluripotent stem cells, with bone marrow-derived MSCs, adipose-derived stem cells, and dedifferentiated chondrocytes. Chondrogenic differentiation was performed in high-density pellet cultures with short-term or long-term TGFβ3 treatment. Chondrogenic gene arrays, gene regulatory networks, and gene ontology analysis revealed divergent signaling pathways. Bulk RNA sequencing was performed to characterize the transcriptomic profiles of each MSC. Results showed that iMSCs produced cartilage with hyaline-like features and minimal hypertrophy, distinguishing them phenotypically from adult MSCs. Gene regulatory network analyses identified EGF, FGFR, FLT1, and HIFA as iMSC hub genes for chondrogenic differentiation. Molecular signaling analysis unveiled that TGFβ3 induced SMAD2/3, not SMAD1/5, suppressing hypertrophy in iMSC chondrogenesis. RNA sequencing highlighted cell-specific differences, functional heterogeneity, and divergent cell signaling profile
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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