Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Phenotypic alterations and PI3K-AKT pathway regulation in senescence of human tonsil mesenchymal stem cells

Qiu X., Lin Z., Sun Y., Zhao A., Chen X.

Laboratory Study, published in Stem Cell Res Ther (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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
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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
Stem Cell Res Ther (2026)
Reported sample size
—
Source database
Europe PMC
PMID
41896931
PMCID
PMC13147630
DOI
10.1186/s13287-026-04986-7

Abstract (original English)

Background Tonsil mesenchymal stem cells (TMSCs) are a promising regenerative medicine source but require continuous subculturing for expansion. Long-term expansion in vitro induces cellular senescence, impairing their function. This study aimed to elucidate senescence-related phenotypic alterations and regulatory mechanisms in human tonsil-derived mesenchymal stem cells. Methods Human-derived TMSCs were isolated from palatine tonsils, cultured under standard conditions, and characterized for mesenchymal markers. Senescence-associated changes were evaluated across early (P1-P5) and late passages (beyond P10). Proliferation capacity was assessed via CCK-8 assays, while senescence-associated β-galactosidase (SA-β-gal) activity and protein levels of p16, p53, and p21 were quantified. RNA sequencing identified differentially expressed genes (DEGs) between young and senescent TMSCs, followed by KEGG pathway enrichment analysis. Key findings were validated by measuring the p-Akt/Akt ratio via Western blot. Results TMSCs showed a progressive decline in proliferative capacity with increasing passages. SA-β-gal staining revealed a significantly higher percentage of positive cells in late-passage TMSCs compared to early-passage cells. Expression levels of P16, P53, and P21 proteins were markedly upregulated in aged TMSCs. KEGG analysis of DEGs indicated significant enrichment in the PI3K

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.

How we grade evidence
Cells, CulturedMesenchymal Stem CellsHumansSignal TransductionCell ProliferationPhenotypeCyclin-Dependent Kinase Inhibitor p16Proto-Oncogene Proteins c-aktPalatine TonsilPhosphatidylinositol 3-Kinases

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