Comprehensive bulk and single-cell RNA sequencing uncovers senescence-associated biomarkers in therapeutic mesenchymal stem cells
Pekker E., Qorri E., Enyedi MZ., Szukacsov V., Ayaydin F., Szabó-Kriston É.
Animal Study, published in Sci Rep (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
- Animal Study
- Journal
- Sci Rep (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41326705
- PMCID
- PMC12783114
- DOI
- 10.1038/s41598-025-30633-x
Abstract (original English)
Mesenchymal stem cells (MSCs) hold great promise in cell therapy, but their effectiveness declines with repeated cell divisions due to senescence. Canines, sharing aging characteristics with humans, serve as a valuable model to study this process in a translational context. In the present study, we performed an in-depth characterization of senescence in canine MSCs using a combination of morphological, molecular, and transcriptomic analyses. Early (P2) and late-passage (P6) canine MSCs were characterized using a combination of senescence-associated β-galactosidase staining, cell cycle profiling, and both bulk and single-cell RNA sequencing to capture global transcriptional changes. By employing a passage-based in vitro approach, the present study demonstrates that late-passage cells (P6) compared to early-passage cells (P2) exhibit hallmark features of senescence, including morphological alterations, elevated SA-β-galactosidase activity, and considerable transcriptional changes. These changes were represented by significant upregulation of established senescence marker genes, alongside potential novel candidates and downregulation of genes associated with cell cycle progression and proliferation. Moreover, single-cell RNA sequencing uncovered heterogeneous distribution of senescent subpopulations, upregulation of SASP-related genes and reduced proliferation markers. Our finding
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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